Immunology - First Aid Flashcards by Grazielle Verzosa | Brainscape

Q

1° Immune System Organs

A

Bone Marrow
Thymus

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Q

2° Immune System Organs

A

Spleen
Lymph Nodes
Tonsils
Peyer Patches

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Q

Immune System Organs:

immune cell production
B cell maturation

A

Bone Marrow

Bone Marrow = B Cell

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Q

Immune System Organs:

T cell maturation

A

Thymus

Thymus = T Cell

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Q

Immune System Organs:

allow immune cells to interact with antigen

A

2° organs:

Spleen
Lymph Nodes
Tonsils
Peyer Patches

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Q

Immune System Organs:

2° lymphoid organ that has many afferents, 1 or more efferents
encapsulated, with trabeculae
functions are nonspecific filtration by macrophages, storage of B and T cells, and immune response activation

A

Lymph Node

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Q

Lymph Node

A

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Q

Lymph Node:

site of B-cell localization and proliferation
outer cortex

A

Follicle

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Q

Lymph Node:

dense
dormant

A

1° follicles

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Q

Lymph Node:

have pale central germinal centers
active

A

2° follicles

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Q

Lymph Node:

consists of cords (closely packed lymphocytes and plasma cells) and sinuses
sinuses communicate with efferent lymphatics and contain reticular cells and macrophages

A

Medulla

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Q

Lymph Node:

houses T cells.
region of cortex between follicles and medulla
contains high endothelial venules through which T and B cells enter from blood
not well developed in patients with DiGeorge syndrome
enlarges in an extreme cellular immune response (eg. viral infection)

A

Paracortex

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Q

Lymphatic Drainage Associations

A

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Q

Lymphatic Drainage Associations:

drains head and neck

A

Cervical

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Q

Lymphatic Drainage Associations:

URTI
Infectious Mononucleosis
Kawasaki disease

A

Cervical

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Q

Lymphatic Drainage Associations:

drains trachea and esophagus

A

Mediastinal

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Q

Lymphatic Drainage Associations:

1° Lung Cancer
Granulomatous disease

A

Mediastinal

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Q

Lymphatic Drainage Associations:

drains lungs

A

Hilar

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Q

Lymphatic Drainage Associations:

Granulomatous disease

A

Hilar

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Q

Lymphatic Drainage Associations:

drains upper limbs, breast, and skin above umbilicus

A

Axillary

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Q

Lymphatic Drainage Associations:

Mastitis
Metastasis (especially breast cancer)

A

Axillary

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Q

Lymphatic Drainage Associations:

drains liver, stomach, spleen, pancreas, and upper duodenum

A

Celiac

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Q

Lymphatic Drainage Associations:

drains lower duodenum, jejunum, ileum, and colon to splenic flexure

A

Superior Mesenteric

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Q

Lymphatic Drainage Associations:

drains colon from splenic flexure to upper rectum

A

Inferior Mesenteric

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Q

Lymphatic Drainage Associations:

Mesenteric Lymphadenitis
Typhoid Fever
Ulcerative Colitis
Celiac disease

A

Celiac
Superior Mesenteric
Inferior Mesenteric

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Q

Lymphatic Drainage Associations:

drains testes, ovaries, kidneys, and uterus

A

Para-aortic

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Q

Lymphatic Drainage Associations:

Metastasis

A

Para-aortic

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Q

Lymphatic Drainage Associations:

drains lower rectum to anal canal (above pectinate line), bladder, vagina (middle third), cervix, and prostate

A

Internal Iliac

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Q

Lymphatic Drainage Associations:

drains anal canal (below pectinate line), skin below umbilicus (except popliteal area), scrotum, and vulva

A

Superficial Inguinal

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Q

Lymphatic Drainage Associations:

Sexually Transmitted Infections

A

Internal Iliac
Superficial Inguinal

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Q

Lymphatic Drainage Associations:

drains dorsolateral foot and posterior calf

A

Popliteal

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Q

Lymphatic Drainage Associations:

Foot/Leg Cellulitis

A

Popliteal

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Q

The right lymphatic duct drains the right side of body above diaphragm into the _____.

A

junction of the right subclavian and internal jugular vein

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Q

The _____ drains everything into the junction of left subclavian and internal jugular veins. Rupture can cause chylothorax.

A

Thoracic Duct

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Q

The spleen is located in the _____ and is protected by _____.

A

LUQ of abdomen, anterior to left kidney

ribs 9-11

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Q

Spleen

A

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Q

Spleen:
long, vascular channels in red pulp with fenestrated “barrel hoop” basement membrane

A

Sinusoids

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Q

Spleen:

T cells are found in the _____ within the white pulp.

A

Periarteriolar Lymphatic Sheath (PALS)

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Q

Spleen:

B cells are found in _____ within the white pulp.

A

follicles

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Q

Spleen:

in between the red pulp and white pulp
contains macrophages and specialized B cells
where antigen-presenting cells (APCs) capture blood-borne antigens for recognition by lymphocytes

A

Marginal Zone

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Q

Splenic macrophages remove _____ bacteria.

A

encapsulated

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Q

Splenic Dysfunction

A

↓ IgM → ↓ complement activation → ↓ C3b opsonization → ↑ susceptibility to encapsulated organisms

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Q

Postsplenectomy Blood Findings

A

Howell-Jolly bodies (nuclear remnants)
Target cells
Thrombocytosis (loss of sequestration and removal)
Lymphocytosis (loss of sequestration)

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Q

You should vaccinate patients undergoing splenectomy against _____.

A

encapsulated organisms

pneumococcal
Hib
meningococcal

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Q

The thymus is located in the _____.

A

anterosuperior mediastinum

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Q

The _____ is an encapsulated organ where T-cells differentiate and mature.

A

Thymus

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Q

The thymus is derived from the _____.

A

3rd pharyngeal pouch

Thymus = Third pharyngeal pouch

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Q

The thymus contains lymphocytes of _____ origin.

A

mesenchymal

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Q

Thymus:

dense with immature T cells

A

Cortex

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Q

Thymus:

pale
mature T cells
Hassall corpuscles containing epithelial reticular cells

A

Medulla

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Q

The normal neonatal thymus is _____ on CXR, involutes with age.

A

“sail-shaped”

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Q

The thymus is hypoplastic in _____.

A

DiGeorge Syndrome
Severe Combined Immunodeficiency (SCID)

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Q

_____ is a neoplasm of thymus. It is associated with myasthenia gravis and superior vena cava syndrome.

A

Thymoma

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Q

Innate Immunity:

Components

A

neutrophils
macrophages
monocytes
dendritic cell
natural killer (NK) cells (lymphoid origin),
complement
physical epithelial barriers
secreted enzymes

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Q

Innate Immunity:

Mechanism

A

germline encoded

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Q

Innate Immunity:

Resistance

A

resistance persists through generations
does not change within an organism’s lifetime

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Q

Innate Immunity:

Response to Pathogens

A

nonspecific
occurs rapidly (minutes to hours)
no memory response

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Q

Innate Immunity:

Secreted Proteins

A

lysozyme
complement
C-reactive protein (CRP)
defensins

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Q

Innate Immunity:

Pathogen Recognition

A

Toll-like receptors (TLRs): pattern recognition receptors that recognize pathogen-associated molecular patterns (PAMPs) and lead to activation of NF-κB
Examples of PAMPs include LPS (gram ⊝ bacteria), flagellin (bacteria), nucleic acids (viruses).

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Q

Adaptive Immunity:

Components

A

T cells
B cells
circulating antibodies

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Q

Adaptive Immunity:

Mechanism

A

variation through V(D)J recombination during lymphocyte development

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Q

Adaptive Immunity:

Resistance

A

microbial resistance not heritable

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Q

Adaptive Immunity:

Response to Pathogens

A

highly specific
refined over time
develops over long periods
memory response is faster and more robust

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Q

Adaptive Immunity:

Secreted Proteins

A

immunoglobulins

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Q

Adaptive Immunity:

Pathogen Recognition

A

Memory cells: activated B and T cells
Subsequent exposure to a previously encountered antigen → stronger, quicker immune response.

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Q

Major histocompatibility complex I and II are encoded by _____.

A

HLA genes

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Q

_____ present antigen fragments to T cells and bind T-cell receptors (TCRs).

A

Major Histocompatibility Complex I and II

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Q

MHC I:

Loci

A

HLA-A
HLA-B
HLA-C

MHC I loci have 1 letter

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Q

MHC I:

Binding

A

TCR
CD8

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Q

MHC I:

Structure

A

1 long chain, 1 short chain

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Q

MHC I:

Expression

A

all nucleated cells, APCs, platelets
not on RBCs

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Q

MHC I:

Function

A

present endogenously synthesized antigens (eg. viral or cytosolic proteins) to CD8+ cytotoxic T cells

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Q

MHC I:

Antigen Loading

A

antigen peptides loaded onto MHC I in RER after delivery via TAP (transporter associated with antigen processing)

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Q

MHC I:

Associated Protein

A

β₂-microglobulin

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Q

MHC II:

Loci

A

HLA-DP
HLA-DQ
HLA-DR

MHC II loci have 2 letters

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Q

MHC II:

Binding

A

TCR
CD4

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MHC II:

Structure

A

2 equal-length chains (2 α, 2 β)

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Q

MHC II:

Expression

A

APCs

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Q

MHC II:

Function

A

present exogenously synthesized antigens (eg. bacterial proteins) to CD4+ helper T cells

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Q

MHC II:

Antigen Loading

A

antigen loaded following release of invariant chain in an acidified endosome

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Q

MHC II:

Associated Protein

A

invariant chain

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Q

HLA Subtypes:

Hemochromatosis

A

A3

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Q

HLA Subtypes:

Addison disease
Myasthenia Gravis
Graves disease

A

B8

Don’t Be late(8), Dr. Addison, or else you’ll send my patient to the grave.

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Q

HLA Subtypes:

Psoriatic Arthritis
Ankylosing Spondylitis,
IBD-associated Arthritis
Reactive Arthritis

A

B27

PAIR

*also known as seronegative arthropathies

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Q

HLA Subtypes:

Celiac disease

A

DQ2/DQ8

I ate (8) too (2) much gluten at Dairy Queen.

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Q

HLA Subtypes:

Multiple Sclerosis
Hay Fever
SLE
Goodpasture Syndrome

A

DR2

Multiple hay pastures have dirt.

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Q

HLA Subtypes:

Diabetes Mellitus Type 1
SLE
Graves disease,
Hashimoto Thyroiditis
Addison disease

A

DR3

2-3, S-L-E

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Q

HLA Subtypes:

Rheumatoid Arthritis
Diabetes Mellitus Type 1
Addison disease

A

DR4

There are 4 walls in a “rheum” (room).

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Q

HLA Subtypes:

Hashimoto Thyroiditis

A

DR5

Hashimoto is an odd doctor (DR3, DR5).

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Q

Natural killer cells are lymphocyte members of the _____.

A

innate immune system

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Q

Natural killer cells use _____ to induce apoptosis of virally infected cells and tumor cells.

A

perforin
granzymes

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Q

Natural killer cells’ activity is enhanced by _____.

A

IL-2
IL-12
IFN-α
IFN-β

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Q

_____ are induced to kill when exposed to a nonspecific activation signal on target cell and/or to an absence of MHC I on target cell surface.

A

Natural Killer Cells

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Q

Natural killer cells kill via _____ (CD16 binds Fc region of bound Ig, activating the NK cell).

A

antibody-dependent cell-mediated cytotoxicity

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Q

Immune Cells:

humoral immunity
recognize antigen—undergo somatic hypermutation to optimize antigen specificity
produce antibody—differentiate into plasma cells to secrete specific immunoglobulins.
maintain immunologic memory—memory _____ persist and accelerate future response to antigen.

A

B Cells

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Q

Immune Cells:

cell-mediated immunity
CD4+ _____ help B cells make antibodies and produce cytokines to recruit phagocytes and activate other leukocytes
CD8+ _____ directly kill virus-infected cells
delayed cell-mediated hypersensitivity (type IV)
acute and chronic cellular organ rejection

A

T Cells

Rule of 8:

MHC II × CD4 = 8
MHC I × CD8 = 8

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Q

Differentiation of T Cells

A

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Q

Differentiation of T Cells:

thymic cortex
T cells expressing TCRs capable of binding self-MHC on cortical epithelial cells survive

A

Positive Selection

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Q

Differentiation of T Cells:

thymic medulla
T cells expressing TCRs with high affinity for self antigens undergo apoptosis or become regulatory T cells
tissue-restricted self-antigens are expressed in the thymus due to the action of autoimmune regulator (AIRE)—deficiency leads to autoimmune polyendocrine syndrome-1

A

Negative Selection

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Q

Th1 cells secrete _____.

A

IFN-γ

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Q

_____ activate macrophages and cytotoxic T cells to kill phagocytosed microbes.

A

Th1 Cells

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Q

Th1 cells are induced by _____.

A

IFN-γ
IL-12

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Q

Th1 cells are inhibited by _____.

A

IL-4
IL-10

*from Th2 cell

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Q

Th1 Cells:

Immunodeficiency

A

Mendelian Susceptibility to Mycobacterial Disease (MSMD)

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Q

Th2 cells secrete _____.

A

IL-4
IL-5
IL-6
IL-10
IL-13

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Q

_____ activate eosinophils and promote production of IgE for parasite defense.

A

Th2 Cells

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Q

Th2 cells are induced by _____.

A

IL-2
IL-4

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Q

Th2 cells are inhibited by _____.

A

IFN-γ

*from Th1 cell

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Q

Th17 cells secrete _____.

A

IL-17
IL-21
IL-22

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Q

_____ provide immunity against extracellular microbes, through induction of neutrophilic inflammation.

A

Th17 Cells

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Q

Th17 cells are induced by _____.

A

TGF-β
IL-1
IL-6

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Q

Th17 cells are inhibited by _____.

A

IFN-γ
IL-4

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Q

Th17 Cells:

Immunodeficiency

A

Hyper-IgE Syndrome

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Q

Treg cells secrete _____.

A

TGF-β
IL-10
IL-35

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Q

_____ prevent autoimmunity by maintaining tolerance to self-antigens.

A

Treg Cells

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Q

Treg cells are induced by _____.

A

TGF-β
IL-2

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Q

Treg cells are inhibited by _____.

A

IL-6

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Q

Treg Cells:

Immunodeficiency

A

IPEX (Immune dysregulation, Polyendocrinopathy, Enteropathy, X-linked) Syndrome

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Q

Immunity:

Th1 cells secrete IFN-γ, which enhances the ability of monocytes and macrophages to kill microbes they ingest.
This function is also enhanced by interaction of T cell CD40L with CD40 on macrophages.

A

Macrophage-Lymphocyte Interaction

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Q

Immunity:

kill virus-infected, neoplastic, and donor graft cells by inducing apoptosis
release cytotoxic granules containing preformed proteins (eg. perforin, granzyme B)
have CD8, which binds to MHC I on virus-infected cells

A

Cytotoxic T Cells

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Q

Immunity:

help maintain specific immune tolerance by suppressing CD4 and CD8 T-cell effector functions
identified by expression of CD3, CD4, CD25, and FOXP3
once activated, they produce anti-inflammatory cytokines (eg. IL-10, TGF-β)

A

Regulatory T Cells (Tregs)

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Q

_____ is caused by the genetic deficiency of FOXP3 → autoimmunity. Characterized by enteropathy, endocrinopathy, nail dystrophy, dermatitis, and/or other autoimmune dermatologic conditions. Associated with diabetes in male infants.

A

IPEX (Immune dysregulation, Polyendocrinopathy, Enteropathy, X-linked) Syndrome

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Q

Antigen-Presenting Cells

A

B Cells
Dendritic Cells
Langerhans Cells
Macrophages

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Q

T Cell Activation

A

Dendritic cell (specialized APC) samples antigen, processes antigen, and migrates to the draining lymph node.
T-cell activation (signal 1): antigen ispresented on MHC II and recognized by TCR on Th (CD4+) cell. Endogenous or cross-presented antigen is presented on MHC I to Tc (CD8+) cell.
Proliferation and survival (signal 2): costimulatory signal via interaction of B7 protein (CD80/86) on dendritic cell and CD28 on naïve T cell.
Th cell activates and produces cytokines. Tc cell activates and is able to recognize and kill virus-infected cell.

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Q

B Cell Activation

A

Th-cell activation as above.
B-cell receptor–mediated endocytosis; foreign antigen is presented on MHC II and recognized by TCR on Th cell.
CD40 receptor on B cell binds CD40 ligand (CD40L) on Th cell.
Th cell secretes cytokines that determine Ig class switching of B cell. B cell activates and undergoes class switching, affinity maturation, and antibody production.

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Q

Antibody Structure

A

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Q

Antibody Function

A

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Q

Antibodies:

_____ (containing the variable/hypervariable regions) consisting of light (L) and heavy (H) chains recognizes antigens.

A

Fab

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Q

Antibodies:

_____ of IgM and IgG fixes complement.

A

Fc region

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Q

Antibodies:

_____ contributes to Fc and Fab regions.

A

Heavy Chain

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Q

Antibodies:

_____ contributes only to Fab region.

A

Light Chain

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Q

Antibodies:

fragment, antigen binding
determines idiotype: unique antigen-binding pocket; only 1 antigenic specificity expressed per B cell

A

Fab

Fragment, antigen binding

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Q

Antibodies:

constant
carboxy terminal
complement binding
carbohydrate side chains
determines isotype (IgM, IgD, etc)

A

Fc

constant
carboxy terminal
complement binding
carbohydrate side chains

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Q

Generation of Antibody Diversity

(antigen independent)

A

random recombination of VJ (light-chain) or V(D)J (heavy-chain) genes
random addition of nucleotides to DNA during recombination by terminal deoxynucleotidyl transferase (TdT)
random combination of heavy chains with light chains

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Q

Generation of Antibody Specificity

(antigen dependent)

A

somatic hypermutation and affinity maturation (variable region)
isotype switching (constant region)

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Q

All immunoglobulin isotypes can exist as _____.

A

monomers

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Q

Mature, naive B cells prior to activation express _____ on their surfaces.

A

IgM
IgD

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Q

Mature, naive B cells may differentiate in germinal centers of lymph nodes by isotype switching (gene rearrangement; induced by cytokines and CD40L) into plasma cells that secrete _____.

A

IgA
IgE
IgG

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Q

Immunoglobulin Isotypes:

main antibody in 2° response to an antigen
most abundant isotype in serum
fixes complement, opsonizes bacteria, neutralizes bacterial toxins an viruses
only isotype that crosses the placenta (provides infants with passive immunity)

A

IgG

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Q

Immunoglobulin Isotypes:

prevents attachment of bacteria and viruses to mucous membranes; does not fix complement
monomer (in circulation) or dimer (with J chain when secreted)
crosses epithelial cells by transcytosis
produced in GI tract (eg. by Peyer patches) and protects against gut infections (eg. Giardia)
most produced antibody overall, but has lower serum concentrations
released into secretions (tears, saliva, mucus) and breast milk
picks up secretory component from epithelial cells, which protects the Fc portion from luminal proteases

A

IgA

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Q

Immunoglobulin Isotypes:

produced in the 1° (immediate) response to an antigen
fixes complement
cannot cross the placenta
antigen receptor on the surface of B cells
monomer on B cell, pentamer with J chain when secreted
pentamer enables avid binding to antigen while humoral response evolves

A

IgM

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Q

Immunoglobulin Isotypes:

unclear function
found on surface of many B cells and in serum

A

IgD

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Q

Immunoglobulin Isotypes:

binds mast cells and basophils; cross-links when exposed to allergen, mediating immediate (type I) hypersensitivity through release of inflammatory mediators such as histamine
contributes to immunity to parasites by activating eosinophils
lowest concentration in serum

A

IgE

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Q

Antigen Type and Memory:

antigens lacking a peptide component (eg. lipopolysaccharides from gram ⊝ bacteria)
cannot be presented by MHC to T cells
weakly immunogenic
vaccines often require boosters and adjuvants (eg. pneumococcal polysaccharide vaccine)

A

Thymus-Independent Antigens

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Q

Antigen Type and Memory:

antigens containing a protein component (eg. diphtheria vaccine)
class switching and immunologic memory occur as a result of direct contact of B cells with Th cells

A

Thymus-Dependent Antigens

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Q

_____ is a system of hepatically synthesized plasma proteins that play a role in innate immunity and inflammation.

A

Complement

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Q

Membrane Attack Complex (MAC) defends against _____.

A

gram ⊝ bacteria

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Q

Complement Activation Pathways:

IgG or IgM mediated

A

Classic

GM makes classic cars.

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Q

Complement Activation Pathways:

microbe surface molecules

A

Alternative

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Q

Complement Activation Pathways:

mannose or other sugars on microbe surface

A

Lectin

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Q

Complement Activation Pathways

A

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Q

Complement Functions:

opsonization

A

C3b

C3b binds bacteria.

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Q

Complement Functions:

anaphylaxis

A

C3a
C4a
C5a

C3a, C4a, C5a = anaphylaxis

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Q

Complement Functions:

neutrophil chemotaxis

A

C5a

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Q

Complement Functions:

cytolysis by MAC

A

C5b-9

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Q

C3b and IgG are the two 1° _____ in bacterial defense; enhance phagocytosis. C3b also helps clear immune complexes.

A

Opsonins

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Q

_____ like decay-accelerating factor (DAF, aka CD55) and C1 esterase inhibitor help prevent complement activation on self cells (eg. RBCs).

A

Inhibitors

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Q

Complement Protein Peficiencies

A

Early Complement Deficiencies (C1-C4)
Terminal Complement Deficiencies (C5–C9)

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Q

Complement Disorders:

increased risk of severe, recurrent pyogenic sinus and respiratory tract infections
increased risk of SLE

A

Early Complement Deficiencies (C1-C4)

Q

Complement Disorders:

increased susceptibility to recurrent Neisseria bacteremia

A

Terminal Complement Deficiencies (C5–C9)

Q

Complement Regulatory Protein Deficiencies

A

C1 Esterase Inhibitor Deficiency
Paroxysmal Nocturnal Hemoglobinuria

Q

Complement Disorders:

causes hereditary angioedema due to unregulated activation of kallikrein → ↑ bradykinin
characterized by ↓ C4 levels
ACE inhibitors are contraindicated

A

C1 Esterase Inhibitor Deficiency

Q

Complement Disorders:

a defect in the PIGA gene preventing the formation of anchors for complement inhibitors, such as decay-acclerating factor (DAF/CD55) and membrane inhibitor of reactive lysis (MIRL/CD59)
causes complement-mediated lysis of RBCs

A

Paroxysmal Nocturnal Hemoglobinuria

Q

Interleukins

A

“Hot T-bone stEAK”:

IL-1: fever (hot)
IL-2: stimulates T cells
IL-3: stimulates bone marrow
IL-4: stimulates IgE production
IL-5: stimulates IgA production
IL-6: stimulates aKute-phase protein production

Q

Cytokines Secreted by Macrophages

A

Interleukin-1
Interleukin-6
Interleukin-8
Interleukin-12
Tumor Necrosis Factor-α

Q

Cytokines Secreted by Macrophages:

causes fever, acute inflammation
activates endothelium to express adhesion molecules
induces chemokine secretion to recruit WBCs
also known as osteoclast-activating factor

A

Interleukin-1

Q

Cytokines Secreted by Macrophages:

causes fever
stimulates production of acutephase proteins

A

Interleukin-6

Q

Cytokines Secreted by Macrophages:

major chemotactic factor for neutrophils

A

Interleukin-8

“Clean up on aisle 8.”

Neutrophils are recruite by IL-8 to clear infections.

Q

Cytokines Secreted by Macrophages:

induces differentiation of T cells into Th1 cells
activates NK cells

A

Interleukin-12

Q

Cytokines Secreted by Macrophages:

activates endothelium
causes WBC recruitment, vascular leak
causes cachexia in malignancy
maintains granulomas in TB

A

Tumor Necrosis Factor-α

Q

_____ are cytokines that can mediate fever and sepsis.

A

IL-1
IL-6
TNF-α

Q

Cytokines Secreted by All T Cells

A

Interleukin-2
Interleukin-3

Q

Cytokines Secreted by All T Cells:

stimulates growth of helper, cytotoxic, and regulatory T cells, and NK cells

A

Interleukin-2

Q

Cytokines Secreted by All T Cells:

supports growth and differentiation of bone marrow stem cells
functions like GM-CSF

A

Interleukin-3

Q

Cytokines from Th1 Cells

A

Interferon-γ

Q

Cytokines from Th1 Cells:

secreted by NK cells and T cells in response to antigen or IL-12 from macrophages
stimulates macrophages to kill phagocytosed pathogens
inhibits differentiation of Th2 cells
activates NK cells to kill virus-infected cells
increases MHC expression and antigen presentation by all cells

A

Interferon-γ

Q

Cytokines from Th2 Cells

A

Interleukin-4
Interleukin-5
Interleukin-10

Q

Cytokines from Th2 Cells:

induces differentiation of T cells into Th (helper) 2 cells
promotes growth of B cells
enhances class switching to IgE and IgG

A

Interleukin-4

Ain’t too proud 2 BEG 4 help.

Q

Cytokines from Th2 Cells:

promotes growth and differentiation of B cells
enhances class switching to IgA
stimulates growth and differentiation of eosinophils

A

Interleukin-5

Q

Cytokines from Th2 Cells:

attenuates inflammatory response
decreases expression of MHC class II and Th1 cytokines
inhibits activated macrophages and dendritic cells
also secreted by regulatory T cells

A

Interleukin-10

TGF-β and IL-10 both attenuate the immune response.

Q

Immunity:

involves the activation of the phagocyte NADPH oxidase complex (eg. in neutrophils, monocytes), which utilizes O₂ as a substrate
plays an important role in the immune response → rapid release of reactive oxygen species (ROS)
NADPH plays a role in both the creation and neutralization

A

Respiratory Burst

(Oxidative Burst)

Q

_____ contains a blue-green heme-containing pigment that gives sputum its color.

A

Myeloperoxidase

Q

Respiratory Burst

(Oxidative Burst)

A

Q

Phagocytes of patients with _____ can utilize H₂O₂ generated by invading organisms and convert it to ROS. Patients are at ↑ risk for infection by catalase ⊕ species (eg. S. aureus, Aspergillus) capable of neutralizing their own H₂O₂, leaving phagocytes without ROS for fighting infections.

A

Chronic Granulomatous Disease

Q

_____ of P. aeruginosa generates ROS to kill competing pathogens.

A

Pyocyanin

Q

Oxidative burst leads to _____, which releases lysosomal enzymes from proteoglycans.

A

K⁺ influx

Q

_____ is a protein found in secretory fluids and neutrophils that inhibits microbial growth via iron chelation.

A

Lactoferrin

Q

Immunity:

part of innate host defense against both RNA and DNA viruses
glycoproteins synthesized by virus-infected cells that act on local cells, “priming them” for viral defense by downregulating protein synthesis to resist potential viral replication and upregulating MHC expression to facilitate recognition of infected cells

A

Interferon-α and -β

Interfere with viruses.

Q

Cell Surface Proteins:

T Cells

A

TCR (binds antigen-MHC complex)
CD3 (associated with TCR for signal transduction)
CD28 (binds B7 on APC)

Q

Cell Surface Proteins:

Helper T Cells

A

CD4
CD40L
CXCR4/CCR5 (co-receptor for HIV)

Q

Cell Surface Proteins:

Cytotoxic T Cells

A

CD8

Q

Cell Surface Proteins:

Regulatory T Cells

A

CD4
CD25

Q

Cell Surface Proteins:

B Cells

A

Ig (binds antigen)
CD19
CD20
CD21 (receptor for EBV)
CD40
MHC II
B7

You can drink Beer at the Bar when you’re 21: B cells, Epstein-Barr virus, CD21.

Q

Cell Surface Proteins:

Macrophages

A

CD14 (receptor for PAMPs, eg. LPS)
CD40
CCR5
MHC II
B7 (CD80/86)
Fc and C3b receptors (enhanced phagocytosis)

Q

Cell Surface Proteins:

NK Cells

A

CD16
CD56 (suggestive marker for NK)

Q

Cell Surface Proteins:

Hematopoietic Stem Cells

A

CD34

Q

_____ is the state during which a cell cannot become activated by exposure to its antigen. This seen in T and B cells when exposed to their antigen without costimulatory signal (signal 2). Another mechanism of self-tolerance.

A

Anergy

Q

Immunity:

receiving preformed antibodies
rapid onset
short span of antibodies (half-life = 3 weeks)

A

Passive

Q

Immunity:

IgA in breast milk
maternal IgG crossing placenta
antitoxin
humanized monoclonal antibody

A

Passive

Q

Immunity:

exposure to foreign antigens
slow onset
long-lasting protection (memory)

A

Active

Q

Immunity:

natural infection
vaccines
toxoid

A

Active

Q

After exposure to _____, unvaccinated patients are given preformed antibodies (passive).

A

“Diseases To Be Healed Very Rapidly”

Diphtheria toxin
Tetanus toxin
Botulinum toxin
HBV
Varicella
Rabies virus

Q

Combined passive and active immunizations can be given for _____ exposure.

A

Hepatitis B
Rabies

Q

Vaccines:

microorganism loses its pathogenicity but retains capacity for transient growth within inoculated host
induces cellular and humoral responses

A

Live Attenuated Vaccine

Q

_____ vaccines can be given to HIV ⊕ patients without evidence of immunity if CD4 cell count ≥ 200 cells/mm³.

A

MMR
Varicella

Q

Vaccines:

Pros of Live Attenuated Vaccine

A

induces strong, often lifelong immunity

Q

Vaccines:

Cons of Live Attenuated Vaccine

A

may revert to virulent form
often contraindicated in pregnancy and immunodeficiency

Q

Live Attenuated Vaccines

A

“Attention! Please Vaccinate Small, Beautiful Young Infants with MMR Regularly!”

Adenovirus (nonattenuated, given to military recruits)
Polio (Sabin)
Varicella (chickenpox)
Smallpox
BCG
Yellow fever
Influenza (intranasal)
MMR
Rotavirus

Q

Vaccines:

pathogen is inactivated by heat or chemicals
maintaining epitope structure on surface antigens is important for immune response
mainly induces a humoral response

A

Killed or Inactivated Vaccine

Q

Vaccines:

Pros of Killed or Inactivated Vaccine

A

safer than live vaccines

Q

Vaccines:

Cons of Killed or Inactivated Vaccine

A

weaker immune response
booster shots usually required

Q

Killed or Inactivated Vaccines

A

RIP Always

Rabies
Influenza (injection)
Polio (Salk)—SalK = Killed
Hepatitis A

Q

Vaccines:

includes only the antigens that best stimulate the immune system

A

Subunit Vaccine

Q

Vaccines:

Pros of Subunit Vaccine

A

lower chance of adverse reactions

Q

Vaccines:

Cons of Subunit Vaccine

A

expensive
weaker immune response

Q

Subunit Vaccines

A

HBV (antigen = HBsAg)
HPV (types 6, 11, 16, and 18)
acellular Pertussis (aP)
Neisseria meningitidis (various strains)
Streptococcus pneumoniae
Haemophilus influenzae type b

Q

Vaccines:

denatured bacterial toxin with an intact receptor binding site
stimulates the immune system to make antibodies without potential for causing disease

A

Toxoid

Q

Vaccines:

Pros of Toxoid

A

protects against the bacterial toxins

Q

Vaccines:

Cons of Toxoid

A

antitoxin levels decrease with time
may require a booster

Q

Toxoids

A

Clostridium tetani
Corynebacterium diphtheriae

Q

Hypersensitivity Types

A

ABCD

Anaphylactic and Atopic (type I)
AntiBody-mediated (type II)
Immune Complex (type III)
Delayed (cell-mediated, type IV)

*Types I, II, and III are all antibody-mediated.

Q

Type I Hypersensitivity

Anaphylactic and Atopic

A

Immediate (minutes): antigen crosslinks preformed IgE on presensitized mast cells → immediate degranulation → release of histamine (a vasoactive amine) and tryptase (a marker of mast cell activation).
Late (hours): chemokines (attract inflammatory cells, eg. eosinophils) and cytokines (eg. leukotrienes) from mast cells → inflammation and tissue damage.

First (type) and Fast (anaphylaxis).

Q

Tests for Type I Hypersensitivity

A

skin test or blood test (ELISA) for allergen-specific IgE

Q

Type II Hypersensitivity

Antibody-Mediated

A

Antibodies bind to cell-surface antigens → cellular destruction, inflammation, and cellular dysfunction.
Cellular Destruction—cell is opsonized (coated) by antibodies, leading to either:
- Phagocytosis and/or activation of complement system.
- NK cell killing (antibody-dependent cellular cytotoxicity).
Inflammation—binding of antibodies to cell surfaces → activation of complement system and Fc receptor-mediated inflammation.
Cellular Dysfunction—antibodies bind to cell surface receptors → abnormal blockade or activation of downstream process.

Q

Tests for Type II Hypersensitivity

A

Direct Coombs test—detects antibodies attached directly to the RBC surface.
Indirect Coombs test—detects presence of unbound antibodies in the serum

Q

Examples of Type II Hypersensitivity

A

Autoimmune Hemolytic Anemia
Immune Thrombocytopenia
Transfusion Reactions
Hemolytic Disease of the Newborn
Goodpasture Syndrome
Rheumatic Fever
Hyperacute Transplant Rejection
Myasthenia Gravis
Graves Disease
Pemphigus Vulgaris

Q

Type III Hypersensitivity

Immune Complex

A

Immune complex—antigen-antibody (mostly IgG) complexes activate complement, which attracts neutrophils; neutrophils release lysosomal enzymes.
Can be associated with vasculitis and systemic manifestations.

In type III reaction, imagine an immune complex as 3 things stuck together: antigen-antibody-complement.

Q

Hypersensitivity Reactions:

the prototype immune complex disease
antibodies to foreign proteins are produced and 1–2 weeks later, antibody-antigen complexes form and deposit in tissues → complement activation → inflammation and tissue damage
fever, urticaria, arthralgia, proteinuria, lymphadenopathy occur 1–2 weeks after antigen exposure

A

Serum Sickness

(Type III Hypersensitivity)

Q

Hypersensitivity Reactions:

a local subacute immune complex-mediated hypersensitivity reaction
intradermal injection of antigen into a presensitized (has circulating IgG) individual leads to immune complex formation in the skin
characterized by edema, necrosis, and activation of complement

A

Arthus Reaction

(Type III Hypersensitivity)

Q

Examples of Type III Hypersensitivity

A

SLE
Polyarteritis nodosa
Poststreptococcal glomerulonephritis

Q

Type IV Hypersensitivity

Delayed

A

Direct Cell Cytotoxicity: CD8+ cytotoxic T cells kill targeted cells.
Inflammatory Reaction: effector CD4+ T cell recognize antigen and release inflammation inducing cytokines (shown in illustration).

4T’s: T cells, Transplant rejections, TB skin tests, Touching (contact dermatitis).

Fourth (type) and last (delayed).

Q

Tests for Type IV Hypersensitivity

A

PPD (tuberculosis infection)
patch test (cause of contact dermatitis)
Candida extract (T cell immune function)

Q

Examples of Type IV Hypersensitivity

A

contact dermatitis (eg. poison ivy, nickel allergy)
graft-versus-host disease

Q

Blood Transfusion Reactions

A

Allergic/Anaphylactic Reaction
Febrile Nonhemolytic Transfusion Reaction
Acute Hemolytic Transfusion Reaction
Transfusion-Related Acute Lung Injury

Q

Blood Transfusion Reactions:

type I hypersensitivity reaction against plasma proteins in transfused blood
IgA deficient individuals must receive blood products without IgA

A

Allergic/Anaphylactic Reaction

Q

Blood Transfusion Reactions:

urticaria
pruritus
fever
wheezing
hypotension
respiratory arrest
shock

A

Allergic/Anaphylactic Reaction

Q

Blood Transfusion Reactions:

within minutes to 2–3 hours

A

Allergic/Anaphylactic Reaction

Q

Blood Transfusion Reactions:

type II hypersensitivity reaction with host antibodies against donor HLA and WBCs
induced by cytokines that are created and accumulate during the storage of blood products

A

Febrile Nonhemolytic Transfusion Reaction

Q

Blood Transfusion Reactions:

fever
headaches
chills
flushing

A

Febrile Nonhemolytic Transfusion Reaction

Q

Blood Transfusion Reactions:

within 1–6 hours

A

Febrile Nonhemolytic Transfusion Reaction

Q

Blood Transfusion Reactions:

type II hypersensitivity reaction
intravascular hemolysis (ABO blood group incompatibility)
extravascular hemolysis (host antibody reaction against foreign antigen on donor RBCs)

A

Acute Hemolytic Transfusion Reaction

Q

Blood Transfusion Reactions:

fever
hypotension
tachypnea
tachycardia
flank pain
hemoglobinuria (intravascular hemolysis)
jaundice (extravascular)

A

Acute Hemolytic Transfusion Reaction

Q

Blood Transfusion Reactions:

within 1 hour

A

Acute Hemolytic Transfusion Reaction

Q

Blood Transfusion Reactions:

donor anti-leukocyte antibodies against recipient neutrophils and pulmonary endothelial cells

A

Transfusion-Related Acute Lung Injury

Q

Blood Transfusion Reactions:

respiratory distress
noncardiogenic pulmonary edema

A

Transfusion-Related Acute Lung Injury

Q

Blood Transfusion Reactions:

within 6 hours

A

Transfusion-Related Acute Lung Injury

Q

Autoantibodies:

Myasthenia Gravis

A

Anti-ACh receptor

Q

Autoantibodies:

Lambert-Eaton Myasthenic Syndrome

A

Anti-Presynaptic Voltage-Gated Calcium Channel

Q

Autoantibodies:

Antiphospholipid Syndrome

A

Anti-β2 Glycoprotein

Q

Autoantibodies:

nonspecific screening antibody
often associated with SLE

A

Antinuclear (ANA)

Q

Autoantibodies:

SLE
Antiphospholipid Syndrome

A

Anticardiolipin
Lupus Anticoagulant

Q

Autoantibodies:

SLE

A

Anti-dsDNA
Anti-Smith

Q

Autoantibodies:

Drug-Induced Lupus

A

Anti-Histone

Q

Autoantibodies:

Mixed Connective Tissue Disease

A

Anti-U1 RNP (ribonucleoprotein)

Q

Autoantibodies:

Rheumatoid Arthritis

A

Rheumatoid Factor (IgM antibody against IgG Fc region)
Anti-CCP (more specific)

Q

Autoantibodies:

Sjögren Syndrome

A

Anti-Ro/SSA
Anti-La/SSB

Q

Autoantibodies:

Scleroderma (diffuse)

A

Anti-Scl-70 (anti-DNA topoisomerase I)

Q

Autoantibodies:

Limited Scleroderma (CREST syndrome)

A

Anticentromere

Q

Autoantibodies:

Polymyositis
Dermatomyositis

A

Antisynthetase (eg. anti-Jo-1)
Anti-SRP
Anti-Helicase (anti-Mi-2)

Q

Autoantibodies:

1° Biliary Cholangitis

A

Antimitochondrial Antibodies

Q

Autoantibodies:

Autoimmune Hepatitis Type 1

A

Anti-Smooth Muscle

Q

Autoantibodies:

Microscopic Polyangiitis
Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss Syndrome)
Ulcerative Colitis

A

MPO-ANCA/p-ANCA

Q

Autoantibodies:

Granulomatosis with Polyangiitis (Wegener)

A

PR3-ANCA/c-ANCA

Q

Autoantibodies:

1° Membranous Nephropathy

A

Anti-Phospholipase A₂ Receptor

Q

Autoantibodies:

Bullous Pemphigoid

A

Anti-Hemidesmosome

Q

Autoantibodies:

Pemphigus Vulgaris

A

Anti-Desmoglein (Anti-Desmosome)

Q

Autoantibodies:

Hashimoto Thyroiditis

A

Antimicrosomal
Antithyroglobulin
Antithyroid Peroxidase

Q

Autoantibodies:

Graves Disease

A

Anti-TSH Receptor

Q

Autoantibodies:

Celiac Disease

A

IgA Anti-Endomysial
IgA Anti-Tissue Transglutaminase
IgA and IgG Deamidated Gliadin Peptide

Q

Autoantibodies:

Type 1 Diabetes Mellitus

A

Anti-Glutamic Acid Decarboxylase
Islet Cell Cytoplasmic Antibodies

Q

Autoantibodies:

Pernicious Anemia

A

Antiparietal Cell
Anti-Intrinsic Factor

Q

Autoantibodies:

Goodpasture Syndrome

A

Anti-Glomerular Basement Membrane

Q

B-Cell Immunodeficiencies

A

X-linked (Bruton) Agammaglobulinemia
Selective IgA Deficiency
Common Variable Immunodeficiency

Q

B-Cell Immunodeficiencies:

defect in BTK, a tyrosine kinase gene → no B-cell maturation
X-linked recessive (↑ in boys)

A

X-linked (Bruton) Agammaglobulinemia

Bruton, BTK, B-cell, Boys

Q

B-Cell Immunodeficiencies:

recurrent bacterial and enteroviral infections after 6 months (↓ maternal IgG)

A

X-linked (Bruton) Agammaglobulinemia

Q

B-Cell Immunodeficiencies:

absent B cells in peripheral blood
↓ Ig of all classes
absent/scanty lymph nodes and tonsils
live vaccines contraindicated

A

X-linked (Bruton) Agammaglobulinemia

Q

B-Cell Immunodeficiencies:

unknown defect
most common 1° immunodeficiency

A

Selective IgA Deficiency

Q

B-Cell Immunodeficiencies:

majority are asymptomatic
airway and GI infections
autoimmune disease
atopy
anaphylaxis to IgA-containing products

A

Selective IgA Deficiency

IgA, Asymptomatic, Airway, Autoimmune, Atopy, Anaphylaxis

Q

B-Cell Immunodeficiencies:

↓ IgA with normal IgG, IgM levels
↑ susceptibility to giardiasis

A

Selective IgA Deficiency

Q

B-Cell Immunodeficiencies:

defect in B-cell differentiation
cause is unknown in most cases

A

Common Variable Immunodeficiency

Q

B-Cell Immunodeficiencies:

usually presents after age 2 and may be considerably delayed
↑ risk of autoimmune disease, bronchiectasis, lymphoma, and sinopulmonary infections

A

Common Variable Immunodeficiency

Q

B-Cell Immunodeficiencies:

↑ plasma cells
↑ immunoglobulins

A

Common Variable Immunodeficiency

Q

T-Cell Immunodeficiencies

A

Thymic Aplasia (DiGeorge Syndrome)
IL-12 Receptor Deficiency
Autosomal Dominant Hyper-IgE Syndrome (Job Syndrome)
Chronic Mucocutaneous Candidiasis

Q

T-Cell Immunodeficiencies:

22q11 deletion
failure of 3rd and 4th pharyngeal pouches to develop → absent thymus and parathyroids

A

Thymic Aplasia (DiGeorge Syndrome)

Q

T-Cell Immunodeficiencies:

tetany (hypocalcemia)
recurrent viral/fungal infections (T-cell deficiency)
conotruncal abnormalities (eg. tetralogy of Fallot, truncus arteriosus)

A

Thymic Aplasia (DiGeorge Syndrome)

Q

T-Cell Immunodeficiencies:

↓ T cells, ↓ PTH, ↓ Ca2+
thymic shadow absent on CXR

A

Thymic Aplasia (DiGeorge Syndrome)

Q

T-Cell Immunodeficiencies:

↓ Th1 response
autosomal recessive

A

IL-12 Receptor Deficiency

Q

T-Cell Immunodeficiencies:

disseminated mycobacterial and fungal infections
may present after administration of BCG vaccine

A

IL-12 Receptor Deficiency

Q

T-Cell Immunodeficiencies:

↓ IFN-γ

A

IL-12 Receptor Deficiency

Q

T-Cell Immunodeficiencies:

deficiency of Th17 cells due to STAT3 mutation → impaired recruitment of neutrophils to sites of infection

A

Autosomal Dominant Hyper-IgE Syndrome (Job Syndrome)

Q

T-Cell Immunodeficiencies:

coarse facies
cold noninflamed staphylococcal abscesses
retained primary teeth
↑ IgE
dermatologic problems (eczema)
bone fractures from minor trauma

A

Autosomal Dominant Hyper-IgE Syndrome (Job Syndrome)

FATED:

coarse Facies
cold (noninflamed) staphylococcal Abscesses
retained primary Teeth
↑ IgE
Dermatologic problems (eczema)

Q

T-Cell Immunodeficiencies:

↑ IgE
↑ eosinophils

A

Autosomal Dominant Hyper-IgE Syndrome (Job Syndrome)

Q

T-Cell Immunodeficiencies:

T-cell dysfunction
can result from congenital genetic defects in IL-17 or IL-17 receptors

A

Chronic Mucocutaneous Candidiasis

Q

T-Cell Immunodeficiencies:
noninvasive Candida albicans infections of skin and mucous membranes

A

Chronic Mucocutaneous Candidiasis

Q

T-Cell Immunodeficiencies:

absent in vitro T-cell proliferation in response to Candida antigens
absent cutaneous reaction to Candida antigens

A

Chronic Mucocutaneous Candidiasis

Q

B-cell and T-Cell Immunodeficiencies

A

Severe Combined Immunodeficiency
Ataxia-Telangiectasia
Hyper-IgM Syndrome
Wiskott-Aldrich Syndrome

Q

B-cell and T-Cell Immunodeficiencies:

several types including defective IL-2R gamma chain (most common, X-linked recessive) and adenosine deaminase deficiency (autosomal recessive)

A

Severe Combined Immunodeficiency

Q

B-cell and T-Cell Immunodeficiencies:

failure to thrive
chronic diarrhea
thrush
recurrent viral, bacterial, fungal, and protozoal infections

A

Severe Combined Immunodeficiency

Q

B-cell and T-Cell Immunodeficiencies:

live vaccines are avoided
given antimicrobial prophylaxis and IVIG
bone marrow transplant is curative (no concern for rejection)

A

Severe Combined Immunodeficiency

Q

B-cell and T-Cell Immunodeficiencies:

↓ T-cell receptor excision circles (TRECs)
absence of thymic shadow (CXR)
absence of germinal centers (lymph node biopsy)
absence of T cells (flow cytometry)

A

Severe Combined Immunodeficiency

Q

B-cell and T-Cell Immunodeficiencies:

defects in ATM gene → failure to detect DNA damage → failure to halt progression of cell cycle → mutations accumulate
autosomal recessive

A

Ataxia-Telangiectasia

Ataxia-Telangiectasia, ATM gene, Ataxia, spider Angiomas, IgA deficiency, ↑ AFP

Q

B-cell and T-Cell Immunodeficiencies:
triad of cerebellar defects (ataxia), spider angiomas
(telangiectasia) and IgA deficiency

A

Ataxia-Telangiectasia

Ataxia-Telangiectasia, ATM gene, Ataxia, spider Angiomas, IgA deficiency, ↑ AFP

Q

B-cell and T-Cell Immunodeficiencies:

↑ AFP
↓ IgA, IgG, and IgE
lymphopenia
cerebellar atrophy
↑ risk of lymphoma and leukemia

A

Ataxia-Telangiectasia

Ataxia-Telangiectasia, ATM gene, Ataxia, spider Angiomas, IgA deficiency, ↑ AFP

Q

B-cell and T-Cell Immunodeficiencies:

most commonly due to defective CD40L on Th cells → class switching defect
X-linked recessive

A

Hyper-IgM Syndrome

Q

B-cell and T-Cell Immunodeficiencies:

severe pyogenic infections early in life
opportunistic infection with Pneumocystis, Cryptosporidium, and CMV

A

Hyper-IgM Syndrome

Q

B-cell and T-Cell Immunodeficiencies:

normal or ↑ IgM
↓↓ IgG, IgA, IgE
failure to make germinal centers

A

Hyper-IgM Syndrome

Q

B-cell and T-Cell Immunodeficiencies:

mutation in WASp gene
leukocytes and platelets unable to reorganize actin cytoskeleton → defective antigen presentation
X-linked recessive

A

Wiskott-Aldrich Syndrome

Q

B-cell and T-Cell Immunodeficiencies:

thrombocytopenia
eczema
recurrent pyogenic infections
↑ risk of autoimmune disease and malignancy

A

Wiskott-Aldrich Syndrome

WATER:

Wiskott-Aldrich
Thrombocytopenia
Eczema
Recurrent (pyogenic) infections

Q

B-cell and T-Cell Immunodeficiencies:

↓ to normal IgG, IgM
↑ IgE, IgA
fewer and smaller platelets

A

Wiskott-Aldrich Syndrome

Q

Phagocyte Dysfunction Immunodeficiencies

A

Leukocyte Adhesion Deficiency (type 1)
Chédiak-Higashi Syndrome
Chronic Granulomatous Disease

Q

Phagocyte Dysfunction Immunodeficiencies:

defect in LFA-1 integrin (CD18) protein on phagocytes
impaired migration and chemotaxis
autosomal recessive

A

Leukocyte Adhesion Deficiency (type 1)

Q

Phagocyte Dysfunction Immunodeficiencies:

recurrent skin and mucosal bacterial infections
absent pus
impaired wound healing
delayed (> 30 days) separation of umbilical cord

A

Leukocyte Adhesion Deficiency (type 1)

Q

Phagocyte Dysfunction Immunodeficiencies:

↑ neutrophils in blood
absence of neutrophils at infection sites

A

Leukocyte Adhesion Deficiency (type 1)

Q

Phagocyte Dysfunction Immunodeficiencies:

defect in lysosomal trafficking regulator gene (LYST)
microtubule dysfunction in phagosome-lysosome fusion
autosomal recessive

A

Chédiak-Higashi Syndrome

Q

Phagocyte Dysfunction Immunodeficiencies:

progressive neurodegeneration
lymphohistiocytosis
albinism (partial)
recurrent pyogenic infections by staphylococci and streptococci
peripheral neuropathy

A

Chédiak-Higashi Syndrome

PLAIN:

Progressive neurodegeneration
Lymphohistiocytosis
Albinism (partial)
recurrent pyogenic Infections by staphylococci and streptococci
peripheral Neuropathy

Q

Phagocyte Dysfunction Immunodeficiencies:

giant granules in granulocytes and platelets
pancytopenia
mild coagulation defects

A

Chédiak-Higashi Syndrome

Q

Phagocyte Dysfunction Immunodeficiencies:

defect of NADPH oxidase → ↓ reactive oxygen species (eg, superoxide) and ↓ respiratory burst in neutrophils
X-linked form most common

A

Chronic Granulomatous Disease

Q

Phagocyte Dysfunction Immunodeficiencies:
↑ susceptibility to catalase ⊕ organisms

A

Chronic Granulomatous Disease

Q

Phagocyte Dysfunction Immunodeficiencies:

abnormal Dihydrorhodamine (flow cytometry) Test (↓ green fluorescence)
Nitroblue Tetrazolium Dye Reduction Test (obsolete) fails to turn blue

A

Chronic Granulomatous Disease

Q

Bacterial Infections in Immunodeficiency:

↓ T Cells

A

Sepsis

Q

Bacterial Infections in Immunodeficiency:

↓ B Cells

A

Encapsulated (Please SHINE my SKiS):

Pseudomonas aeruginosa
Streptococcus pneumoniae
Haemophilus Influenzae type b
Neisseria meningitidis
Escherichia coli
Salmonella
Klebsiella pneumoniae
Group B Streptococcus

Q

Bacterial Infections in Immunodeficiency:

↓ Granulocytes

A

Staphylococcus
Burkholderia cepacia
Pseudomonas aeruginosa
Serratia
Nocardia

Q

Bacterial Infections in Immunodeficiency:

↓ Complement

A

encapsulated species with early complement deficiencies
Neisseria with late complement (C5–C9) deficiencies

Q

Viral Infections in Immunodeficiency:

↓ T Cells

A

CMV
EBV
JC virus
VZV
chronic infection with respiratory/GI viruses

Q

Viral Infections in Immunodeficiency:

↓ B Cells

A

enteroviral encephalitis
poliovirus (live vaccine contraindicated)

Q

Fungal/Parasitic Infections in Immunodeficiency:

↓ T Cells

A

Candida (local)
PCP
Cryptococcus

Q

Fungal/Parasitic Infections in Immunodeficiency:

↓ B Cells

A

GI giardiasis (no IgA)

Q

Fungal/Parasitic Infections in Immunodeficiency:

↓ Granulocytes

A

Candida (systemic)
Aspergillus
Mucor

Q

B-cell deficiencies tend to produce recurrent _____ infections, whereas T-cell deficiencies produce more _____ infections.

A

B-cell → bacterial

T-cell → fungal and viral

Q

Grafts:
from self

A

Autograft

Q

Grafts:
from identical twin or clone

A

Syngeneic Graft (Isograft)

Q

Grafts:

from nonidentical individual of same species

A

Allograft

Q

Grafts:

Xenograft

A

from different species

Q

Transplant Rejection:

onset within minutes

A

Hyperacute

Q

Transplant Rejection:

pre-existing recipient antibodies react to donor antigen (type II hypersensitivity reaction)
activate complement

A

Hyperacute

Q

Transplant Rejection:

widespread thrombosis of graft vessels → ischemia/necrosis
graft must be removed

A

Hyperacute

Q

Transplant Rejection:

onset within weeks to months

A

Acute

Q

Transplant Rejection:

Cellular: CD8+ T cells and/or CD4+ T cells activated against donor MHCs (type IV hypersensitivity reaction)
Humoral: similar to hyperacute, except antibodies develop after transplant

A

Acute

Q

Transplant Rejection:

vasculitis of graft vessels with dense interstitial lymphocytic infiltrate
prevent/reverse with immunosuppressants

A

Acute

Q

Transplant Rejection:

onset within months to years

A

Chronic

Q

Transplant Rejection:

CD4+ T cells respond to recipient APCs presenting donor peptides, including allogeneic MHC
both cellular and humoral components (type II and IV hypersensitivity reactions)

A

Chronic

Q

Transplant Rejection:

recipient T cells react and secrete cytokines → proliferation of vascular smooth muscle, parenchymal atrophy, interstitial fibrosis
dominated by arteriosclerosis

A

Chronic

Q

Transplant Rejection:

Bronchiolitis Obliterans (lung)
Atherosclerosis (heart)
Chronic Graft Nephropathy (kidney)
Vanishing Bile Duct Syndrome (liver)

A

Chronic

Q

Transplant Rejection:

onset varies

A

Graft-Versus-Host Disease

Q

Transplant Rejection:

grafted immunocompetent T cells proliferate in the immunocompromised host and reject host cells with “foreign” proteins → severe organ dysfunction
type IV hypersensitivity reaction

A

Graft-Versus-Host Disease

Q

Transplant Rejection:

maculopapular rash
jaundice
diarrhea
hepatosplenomegaly
usually in bone marrow and liver transplants (rich in lymphocytes)
potentially beneficial in bone marrow transplant for leukemia (graft-versus-tumor effect)

A

Graft-Versus-Host Disease

Q

_____ are agents that block lymphocyte activation and proliferation. Reduce acute transplant rejection by suppressing cellular immunity (used as prophylaxis). Frequently combined to achieve greater efficacy with ↓ toxicity. Chronic suppression ↑ risk of infection and malignancy.

A

Immunosuppressants

Q

Immunosuppressants:

calcineurin inhibitor
binds cyclophilin
blocks T-cell activation by preventing IL-2 transcription

A

Cyclosporine

Q

Immunosuppressants:

Psoriasis
Rheumatoid Arthritis

A

Cyclosporine

Q

Immunosuppressants:

nephrotoxicity
hypertension
hyperlipidemia
neurotoxicity
gingival hyperplasia
hirsutism

A

Cyclosporine

Q

Immunosuppressants:

calcineurin inhibitor
binds FK506 binding protein (FKBP)
blocks T-cell activation by preventing IL-2 transcription

A

Tacrolimus (FK506)

Q

Immunosuppressants:

similar to cyclosporine
↑ risk of diabetes and neurotoxicity
no gingival hyperplasia or hirsutism

A

Tacrolimus (FK506)

Q

Calcineurin inhibitors are highly _____.

A

nephrotoxic

Q

Immunosuppressants:

mTOR inhibitor
binds FKBP
blocks T-cell activation and B-cell differentiation by preventing response to IL-2

A

Sirolimus (Rapamycin)

Q

Immunosuppressants:

pancytopenia
insulin resistance
hyperlipidemia
not nephrotoxic

A

Sirolimus (Rapamycin)

Q

Immunosuppressants:

synergistic with cyclosporine
used in drug-eluting stents

A

Sirolimus (Rapamycin)

Q

Immunosuppressants:

monoclonal antibody
blocks IL-2R

A

Basiliximab

Q

Immunosuppressants:

edema
hypertension
tremor

A

Basiliximab

Q

Immunosuppressants:

specifically for kidney transplant rejection prophylaxis

.

A

Sirolimus (Rapamycin)
Basiliximab

Q

Immunosuppressants:

antimetabolite precursor of 6-mercaptopurine
inhibits lymphocyte proliferation by blocking nucleotide synthesis

A

Azathioprine

Q

Immunosuppressants:

Rheumatoid Arthritis
Crohn disease
Glomerulonephritis
other autoimmune conditions

A

Azathioprine

Q

Immunosuppressants:

pancytopenia

A

Azathioprine

Q

Immunosuppressants:

6-MP degraded by xanthine oxidase
toxicity ↑ by allopurinol

A

Azathioprine

Q

Immunosuppressants:

reversibly inhibits IMP dehydrogenase preventing purine synthesis of B and T cells

A

Mycophenolate Mofetil

Q

Immunosuppressants:

Lupus Nephritis

A

Mycophenolate Mofetil

Q

Immunosuppressants:

GI upset
pancytopenia
hypertension
hyperglycemia
less nephrotoxic and neurotoxic

A

Mycophenolate Mofetil

Q

Immunosuppressants:

associated with invasive CMV infection

A

Mycophenolate Mofetil

Q

Immunosuppressants:

inhibit NF-κB
suppress both B- and T-cell function by ↓ transcription of many cytokines
induce T cell apoptosis

A

Glucocorticoids

Q

Immunosuppressants:

many autoimmune and inflammatory disorders
adrenal insufficiency
asthma
CLL
non-Hodgkin lymphoma

A

Glucocorticoids

Q

Immunosuppressants:

Cushing syndrome
osteoporosis
hyperglycemia
diabetes
amenorrhea
adrenocortical atrophy
peptic ulcers
psychosis
cataracts
avascular necrosis (femoral head)

A

Glucocorticoids

Q

Immunosuppressants:

demargination of WBCs causes artificial leukocytosis
adrenal insufficiency may develop if drug is stopped abruptly after chronic use

A

Glucocorticoids

Q

Immunosuppression

A

Q

Recombinant Cytokines for Bone Marrow Stimulation

A

Erythropoietin
Colony Stimulating Factors
Thrombopoietin

Q

Recombinant Cytokines for Bone Marrow Stimulation:

Epoetin alfa (EPO analog)
used in anemias (especially in renal failure)

A

Erythropoietin

Q

Recombinant Cytokines for Bone Marrow Stimulation:

Filgrastim (G-CSF) and Sargramostim (GM-CSF)
used in leukopenia to recover granulocyte and monocyte counts

A

Colony Stimulating Factors

Q

Recombinant Cytokines for Bone Marrow Stimulation:

Romiplostim (TPO analog) and Eltrombopag (TPO receptor agonist)
used in autoimmune thrombocytopenia

A

Thrombopoietin

Q

Recombinant Cytokines for Immunotherapy

A

Interleukin-2
Interferon

Q

Recombinant Cytokines for Immunotherapy:

Aldesleukin
used in renal cell carcinoma and metastatic melanoma

A

Interleukin-2

Q

Recombinant Cytokines for Immunotherapy:

Interferons

A

IFN-α—Chronic Hepatitis C (not preferred) and B, Renal Cell Carcinoma
IFN-β—Multiple Sclerosis
IFN-γ—Chronic Granulomatous Disease

Q

Therapeutic Antibodies for Cancer Therapy

A

Alemtuzumab
Bevacizumab
Cetuximab
Rituximab
Trastuzumab

Q

Therapeutic Antibodies for Cancer Therapy:

targets CD52
used in CLL and MS

A

Alemtuzumab

“Alymtuzumab”—chronic lymphocytic leukemia

Q

Therapeutic Antibodies for Cancer Therapy:

targets VEGF
used in colorectal cancer, renal cell carcinoma, and non-small cell lung cancer
also used in neovascular agerelated macular degeneration, proliferative diabetic retinopathy, and macular edema

A

Bevacizumab

Q

Therapeutic Antibodies for Cancer Therapy:

targets EGFR
used in stage IV colorectal cancer, head and neck cancer

A

Cetuximab

Q

Therapeutic Antibodies for Cancer Therapy:

targets CD20
usedin B-cell non-Hodgkin lymphoma, CLL, rheumatoid arthritis, ITP, and multiple sclerosis

A

Rituximab

Q

Therapeutic Antibodies for Cancer Therapy:

targets HER2
used in breast cancer and gastric cancer

A

Trastuzumab

HER2—“tras2zumab”

Q

Therapeutic Antibodies for Autoimmune Disease Therapy

A

Adalimumab
Certolizumab
Golimumab
Infliximab
Daclizumab
Eculizumab
Natalizumab
Ustekinumab

Q

Therapeutic Antibodies for Autoimmune Disease Therapy:

targets soluble TNF-α
used inIBD, rheumatoid arthritis, ankylosing spondylitis, and psoriasis

A

Adalimumab
Certolizumab
Golimumab
Infliximab

Q

Therapeutic Antibodies for Autoimmune Disease Therapy:

targets CD25 (part of IL-2 receptor)
used in relapsing multiple sclerosis

A

Daclizumab

Q

Therapeutic Antibodies for Autoimmune Disease Therapy:

targets complement protein C5
used in paroxysmal nocturnal hemoglobinuria

A

Eculizumab

Q

Therapeutic Antibodies for Autoimmune Disease Therapy:

targets α4-integrin—WBC adhesion
used in multiple sclerosis and Crohn disease
risk of PML (progressive multifocal leukoencephalopathy) in patients with JC virus

A

Natalizumab

Q

Therapeutic Antibodies for Autoimmune Disease Therapy:

targets IL-12/IL-23
used in psoriasis and psoriatic arthritis

A

Ustekinumab

Q

Therapeutic Antibodies:

targets platelet glycoproteins IIb/IIIa
antiplatelet agent for prevention of ischemic complications in patients undergoing percutaneous coronary intervention

A

Abciximab

IIb x IIIa equals “absiximab”

Q

Therapeutic Antibodies:

targets RANKL
used in osteoporosis
inhibits osteoclast maturation (mimics osteoprotegerin)

A

Denosumab

Denosumab affects osteoclasts

Q

Therapeutic Antibodies:

targets digoxin
antidote for digoxin toxicity

A

Digoxin immune Fab

Q

Therapeutic Antibodies:

targets IgE
used in refractory allergic asthma
prevents IgE binding to FcεRI

A

Omalizumab

Q

Therapeutic Antibodies:

targets RSV F protein
used as RSV prophylaxis for high-risk infants

A

Palivizumab

PaliVIzumab—VIrus