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immunology Flashcards

1
Q

Immune system organs

A

1’ organs: Bone marrow (immune cell production, B cell maturation), Thymus T cell maturation
2’ organs: Spleen, lymph nodes, tonsils, Peyer patches, Allow immune cells to interact with antigen

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2
Q

Lymph node

A

Many Afferents (from all around the body) and a few or even one efferent.

Encapsulated with trabeculae, functions are non specific filtration by macrophages, circulation of B and T cells, and immune response

Follicle: Site of B cell localization and proliferation, in outer cortex, 1’ follicles are dense and quiescent, 2’ follicles have pale central germinal centers are are active

Medulla: has medullary cords (closely packed lymphocytes and plasma cells) and medullary sinus, the medullary sinuses communicate with efferent lymphatics and contain reticular cells and macrophages

Paracortex: Contains T cells, regions of corTex between follicles and medulla, contains high endothelial venules(where T and B cells come in from blood), not well developed in pt with Digeorge syndrome
Paracortex enlarges in an extreme cell immune response (EBV and other viral infections–> paracortical hyperplasia, lymphadenopathy

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3
Q

Spleen

A

Protected by 9 and 10 ribs
Sinusoids are long, vascular channels in red pulp with fenestrated barrel hoop basement membrane
T cells are found in the periarteriolar lymphatic sheath (kinda like the paracortex in the lymphnode)
B cells are found in the follicles within the White Pulp
The marginal zone, in between the red pulp and white pulp, contains Macrophages and specialized B cells, and its where APCs capture blood born antigens for recognition by lymphocytes

Splenic macrophages remove encapsulated bacteria

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4
Q

Splenic dysfunction

A

post splenectomy, sickle cell disease autosplenectomy
leads to decreased IgM–> low complement activation–> low C3b opsonization–> increased susceptibility to encapsulated organisms

Post splenectomy findings: Howell-Jolley bodies (nuclear remnants), Target cells, Thrombocytosis (loss of sequestration and removal of platelets)
Lymphocytosis (loss of sequestration)

Vaccinate patients undergoing splenectomy or with splenic dysfunction against encapsulated organisms (pneumococci, Hib, meningococcal)

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5
Q

Thymus

A

located in the Anterior superior mediastinum, Site of T cell differentiation and maturation

Encapsulated
Thymus epithelium is derived from Third pharyngeal pouch- endoderm
Thymic lymphocytes are of mesodermal origin

Cortex is dense with immature T cells

Medulla is pale with Mature T cells, and Hassell corpuscles (containing epithelial reticular cells)

Involutes by age 3

Absent thymic shadow or hypoplastic thymus seein in SCID and diGeorge syndrome

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6
Q

Thymoma

A

neoplasm of thymus, associated with myasthenia gravis, SVC syndrome, pure red cell aplasia
Good syndrome

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7
Q

Innate immunity

A

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

Germline encoded

Resistance persists through generations, does not change within an organisms lifetime

response is quick and non specific, (minutes to hours, no memroy

Secrete lysozyme, complement, CRP, defensins, cytokines

Recognition: TLR: pattern recognition receptors (PRRs) that recognize pathogen associated molecular patterns (PAMPs) and lead to activation NFkB

PAMPs: LPS (from gram neg bacteria), Flagellin (bacteria), nucleic acids from viruses

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8
Q

Adaptive immunity

A

T cells, B cells and circulating antibodies

Variation through VDJ recombination during lymphocyte development

Microbial resistance not heritable

Very specific refined over time, memory response is faster and more robust

Secreted: immunoglobulins

Memory cells: activated B and T cells–> subsequent exposure to a previously encountered anitgen–> stronger, quicker immune response

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9
Q

MHC

A

Encoded by HLA genes, present antigens to T cells and bind T cell receptors (TCRs)

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10
Q

MHC 1

A

HLA A B C (1 letter)
Bind to TCR and CD 8
have 1 long chain and 1 short chain
All nucleated cells have it (APCs, platelets), none on RBC
Present endogenous antigens (viral, cytosolic proteins) to CD8 cytotoxic Tcell

Antigen peptides are loaded onto MHC 1 in the RER after delivery via TAP (transporter associated with antigen processing

Associated with the B2 microglobulin

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11
Q

MHC2

A

HLA DP DQ DR (2 letters)
binds TCR and CD4

2 equal length chains (2 a and 2B)
only present on APCs

present exogenous Ags (bacterial proteins to CD4+ helper T cells

AG loaded following release of invariant in an acidified endosome

Invariant chain holds on to MHC 2 with antigen, when released will go on the cytoplasm

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12
Q

NK cells

A

Lymphocyte member of innate immune system
Use perforin and granzyme to induce apoptosis of virally infected cells and tumor cells

Activity is enhanced by IL2, IL12, IFNa, IFNB

Induced to kill when exposed to a nonspecific activation signal on target cell and/or to an absence of MHC1 on a target cell surface

Also kills via antibody-dependent cell mediated cytotoxicity (Cd16 binds the Fc region of bound IgG, Actiivating NK cell)

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13
Q

Major functions of B cells

A

Humoral immunity
Recognize and present Antigen- undergo somativ hypermutation to optimize antigen specifity

Produce antibody- differentiate into plasma cells to secrete specific immunoglobulins

Maintain immunologic memory (memory B cells persist and accelerate future response to Antigen)

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14
Q

T cells

A

Cell mediated immunity

CD4 T cells help B cells make antibodies and produce cytokines to recruite phagocytes and activate other leukocytes

CD8 T cells kill virus-infected and tumor cells via perforin and granzymes (similar to NK cell)

Delayed cell mediated hypersensitibvity (type 4

Acute and chronic cellular organ rejection

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15
Q

Differentiation of T cells

A

Immature T cells from Bone marrow travel to thymus cortex

  • Thymic cortex- positive selection occurs (CD8 + and CD4+ T cells expressing TCRs capable of binding self-MHC on cortical epithelial cells survive) Some become CD8 and some become CD4
  • Thymic medulla: Negative selection T cells expressing TCRs with very 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 the AIRE (autoimmune regulatory) deficiency leads to inability to express self antigens during negative selection–> no negative selection deficiency leads to Autoimmune polyendocrine syndrome 1: Chronic mucocutaneous candidiasis, Hypoparathyroidism, Adrenal insufficiency, Recurrent candida infections)

Then the CD4 and CD8 cells go the the lymph nodes ( paracorTex)

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16
Q

What are the 4 types of CD4 T helper cells

A

Th1 (activated by IFNy, IL12 inhibited by IL4, IL10)
Th2 (activated by IL2 and IL4 inhibited by IFNy)
Th 17 (activated by TGFB, IL1, IL6 inhibited by IFNy, IL4)
T reg ( Activated by TGF B, IL2, and activated by IL6)

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17
Q

Macrophage -lymphocyte interaction

A

Th1 cells secrete IFNy, enhances the ability of monocytes and macrophages to kill microbes, also enhanced by CD40L (on Tcell) and CD40 on Macrophages

Macrophages also activate lymphocytes via antigen presentation

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18
Q

Cytotoxic T cell

A

Kills virus, tumor, donor graft cells, by inducing apoptosis, release cytotoxic granules containing preformed proteins (perforin granzyme B), Cytotoxic T cells have CD8

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19
Q

Treg cells

A

help maintain immune tolerance by CD4 and CD8 T effector functions
Identified by expression of CD3 CD4 CD25 and FOXP3

Acitvated Tregs produce anti-inflammatory cytokines (IL10, TGFB)

IPEX- immune dysregulation, Polyendocrinopathy, Enteropathy, X linked syndrome

Genetic deficiency of FOX P3–> autoimmunity , diabetes in male infants

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20
Q

T and B cell activation

A 
APCs: B cells, dendritic cells, Langerhans cells, macrophages
2 signals are required for T cell activation, B cell activation, and class switching
21
Q

T cell activation

A

1 Dendritic cell (specialized APC) samples and processes antigens, then migrates to the draining lymph node (grabs a chunk of antigen)

  1. T cell activation (signal 1) exogenous antigen is presented on MHC 2 and recognized by TCR on Th CD4 T cell. Endogenous is presented on MHC 1 CD8 T cell
  2. Proliferation and survival (signal 2): costimulatory signal via the interaction of B7 protein (CD80/86) on DC and CD28 (receptor) on the naiive T cell
  3. Activated Th Cell produces cytokines, Tc cell able to recognize and kill virus-infected cell
22
Q

B cell activation and class switching

A
  1. Th cell activation (via T cell activation from previous card)
  2. B-cell receptor-mediated mediated endocytosis of the antigen
  3. Exogenous antigen is presented on MHC2 and recognized by TCR on Th cell
  4. CD40 receptor on the B cell and CD40L on Th cell bind
  5. Th cells secrete cytokines that determine Ig class switching of B cells
  6. B cells are activated, undergo class switching and affinity maturation and become Plasma cells that secrete antibodies
23
Q

Antibody Structure and function

A

Fab (containing the variable/ hyper variable region) ab for specific Antibody

consists of Light chain and heavy chain, recognizes antigens

Fc region of IgM and IgG fixes complement. Heavy chain contributes to Fc and Fab regions, Light chain is only Fab and hypervariable

Fab: Fragment, antigen binding: determines idiotype (unique Ag binding pocket, only one antigenic specificity expressed per B cell)

Fc (5Cs): Constant, Carboxy terminal, Complement binding, Carbohydrate side chains, Confers (determines)- isotype (IgM IgD)

24
Q

Generation of Ab diversity (antigen independent)

A

Random recombination of VJ (light chain) or VDJ (heavy chain)

Random addition of nucleotides to DNA during recombination by terminal deoxynucleotidyl transferase (TdT)

Random combination of heavy chains with light chains

25
Q

Generation of antibody specificity (antigen dependent)

A 
Somatic hypermutation and affinity maturation in the variable region)
Isotype switching (constant region)
26
Q

Immunoglobulin isotypes

A

All isotypes can exist as monomers, Mature, naiive B cells prior to activation express IgM and IgD on their surfaces

They may differentiate in germinal centers of lymph nodes by isotype switching (gene rearrangement induced by Cytokines CD40L) into plasma cells that secrete IgA, E or G

Affinity refers to the antibody antigen interaction. Avidity is the cumulative binding strength of all antibody-antigen interaction in a multivalent molecule (LPS or bacteria has high avidity)

27
Q

IgG

A

Main antibody 2’ response to an antigen, most abundant isotype in serum. Fixes complement, opsonizes bacteria, neutralizes bacterial toxins and viruses.
Only isotype that crosses the placenta
Provides infants with passive immunity that starts to wane after birth

IgG Greets Growing fetus

28
Q

IgA

A

Prevents attachment of Bacteria and viruses to mucous membranes, does not fix complement
Monomer in circulation
Dimer (with J chain when secreted)
Crosses epithelial cells by transcytosis
Produced in GI tract by Peyer patches and protects against gut infections (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

29
Q

IgM

A

Produced in the 1’ immediate response to an antigen, fix complement, Ag receptor on the surface of B cells, Monomer on B cell, pentamer in crculation, Pentamer allows for avid binding to Ag while humoral response evolves

30
Q

IgE

A

Binds mast cells and basophils, cross links when exposed to allergen, mediating immediate (type 1) hypersensitivity through release of inflammatory mediators such as histamine
Contributes to immunity to parasites by activating eosinophils

31
Q

Antigen type and memory

A

Thymus-independent antigens: Antigens lacking a peptide component (LPS, gram negative bacteria) cannot be presented by MHC to T cells Weakly immunogenic , vaccines require boosters and adjuvants

Thymus dependent: Antiges containing a protein component (Strep pneumo PCV, poly saccharides conjugated to diptheria toxin like protein) class switching and immunologic memory occur as class switching and immunologic memory can occur

32
Q

Complement

A

System of hepatically synthesized plasma proteins that play a role in innate immunity and inflammation

MAC defends against gram - bacteria, the CH50 test is used to screen for activation of classic complement pathway.

33
Q

Complement activation pathways

A

Classic pathway (IgG or IgM mediated) GM makes classic cars

Alternative- microbe surface markers

Lectin-mannose (other sugars) on microbe surface

all will lead to C3b–> C5-> C5b-9 (MAC)

C3b-opsonization (binds to bacteria)
C3a C4a C5a- Anaphylaxis
C5a- neutrophil chemotaxis

34
Q

Opsonins

A

C3b and IgG are the 2 1’ opsonins in bacterial defense, enhance phagocytosis. C3b also helps clear immune complexes

35
Q

Inhibitors

A

decay accelerating factor (DAF) aka CD55

and CD1 esterase inhibitor help prevent complement activation on self cells

36
Q

Early complement deficiencies

A

Increased risk of severe, recurrent pyogenic sinus and respiratory tract infections

Increased risk of SLE

37
Q

Late complement deficiences

A

increased susceptibility to recurrent Neisseria bacteremia

38
Q

C1 esterase inhibitor deficiency

A

Causes hereditary angioedema due to unregulated activation of kallikrein–> increased bradykinin
Characterized by decreased Cd4 levels

ACE inhibitors are contraindicated (because they also cause a release of brady kinin)

39
Q

Paroxysmal nocturnal hemoglobinuria

A

A defect in the PIGA gene preventing the formation of glycosylphosphatidylinosotol (GPI) anchors for complment inhibitors such as decay accelerating factor DAF and CD55 and membrane inhibitor of reactive lysis (MIRL CD59)

Causes of complement mediated intravascular hemolysis–> decreased haptoglobin and dark urine

40
Q

Cytokines that cause acute inflammation

A

Acute: IL1, IL6, TNFa

Then recruit IL8, IL12

41
Q 
IL 1
IL2
IL 3
IL4 
IL 6
A 
HOT T BONE st E A K
IL1: Hot (fever)
IL2: Stimulates T cells
IL 3: Stimulates Bone marrow
IL 4: IgE production
IL 5: IgA production
IL 6: stimulates aKute phase protein production
42
Q

Antiinflammatory cytokines

A

TGF B and IL 10

TGF B and IL 10 Both atTENuate the immune response

43
Q

Respiratory burst

A

Also called the oxidative burst:
Involves the activation of the phagocyte NADPH oxidase complex (in PMNs and macrophages), which utilize O2 as a substrate

Plays an important role in the immune response–> rapid release of reactive oxygen species

NADPH plays a role in both the creation and neutralization of ROS

Myeloperoxidase contains a blue-green, heme containing pigment that gives the sputum its color (thats why bleach is kinda green/blue)

44
Q

Chronic granulomatous disease

A

There are many paths from H202

O2-> NADPH oxidase (O2-) –> Superoxide dismutase (H202) –> Myeloperoxidase (HOCl bleach)–> kills the organism)

O2-> NADPH oxidase (O2-) –> Superoxide dismutase (H202) –> used by bacterial catalase to avoid killing –> H20 and O2

O2-> NADPH oxidase (O2-) –> Superoxide dismutase (H202) –> Glutathione GSH (H20) + GSSG–> Taken with NADPH via Glutathione reductase–> NADP+ with G6P –> 6 phosphogluconolactone via G6PD ***Egyptians

45
Q

Type 1 Hypersensitivity

A

Anyphylactic and Atopic
2 phases:
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 actiation)

Late (hours): chemokines (attract inflammatory cells like eosinophils and other mediators, leukotrienes from mast cells–> inflammation and tissue damage

First (type) and Fast (anaphylaxis)

Test: skin test or ELISA blood test for allergen specific IgE
Allergic asthma

46
Q

Type 2 hypersensitivity

A

Antibodies bind to cell surface antigens–> cell destruction, inflammation, and cellular dysfunction

Cell destruction: cell is opsonized by Ab leading to either Phagocytosis and or activation of complement. OR NK cell killing (Ab-dependent cell cytotoxicity

Inflammation- binding of Ab to cell surface–> activation of complement system and Fc receptor mediated inflammation

Cell dysfunction - Anitbodies bind to cell surface receptors–> abnormal blockade or activation of downstream process

Direct Coombs test - detects Ab attached directly to RBCs

Indirect Coombs detects precence of unbound Ab in the serum

47
Q

Type 3 Hypersensitivy

A

Immune complex

Ag-Ab (mostly IgG)- complex activate complement, which attracts PMNs, which release lysosomal enzyme
Can be associated with vasculitis and systemic manifestation

Serum Sickness- the prototypic immune complex disease, Ab to foreign proteins are produced and 1-2 weeks later Ab-Ag Complexes form and deposit in tissue–> complement activation –> inflammation and tissue damage

Arthus reaction- a local subacute immune complex-mediated HS reactivity - Edema necrosis and activation of complement

Ag-Ab activating complex

48
Q

Type 4 HS

A

envolve delayed T cell tesponse

Direct cytotoxicity- CD8 T cells kill target cells
Inflammatory reaction- effector CD4 T cells recognize Ag and release inflammation-inducing cytokines

Contact dermatitis
Graft vs host
PPD for TB test

First aid (12 decks)

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