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Pathophysiology > eRobbins Ch 4 - Diseases of the Immune System > Flashcards

eRobbins Ch 4 - Diseases of the Immune System Flashcards

1
Q

Innate Immunity

A

Natural/Native immunity

Mediated by cells/proteins that are always present & poised to fight

Immediate

Epithelial barriers (mucosa, skin, respiratory tract, GI tract)
Phagocytes (Neutrophils & Macrophages)
NK Cells
Compliment Cascade -> INFLAMMATION

Cytokine: IL 12, IFN-gamma, IL-23, TNF-alpha & IL-1

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2
Q

Adaptive Immuntiy

A

Acquired/Specific Immunity
Specialized APC

Humoral & Cell Mediated Immunity

B Lymphocytes = antibodies
T Lymphocytes = Helper or attack cells

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3
Q

Humoral Immunity

A

Antibodies bind to microbes & tag them for removal

Antibodies = Soluble proteins produced by B Lymphocytes/B Cells

Antibodies attack EXTRACELLULAR microbes in the blood (attach to outside of free floating microbes/peptides)

Effector cell = plasma cells that secrete antibodies

BACTERIAL

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4
Q

Cell-Mediated Immunity

A

Medicated by T Cells/Lymphocytes

Designed to phagocytose infected cells = VIRUSES

Cytotoxic T Lymphocytes (CTL) = Directly kill infected cells

Helper T Cells = activate phagocytes (to phagocytose microbes & then kill) via cytokines

Effector Cell = CTL mostly, but also Helper T Cells

Naive T cells are activated by antigen & co-stimulators to proliferate & differentiate

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5
Q

T Lymphocytes

A

Thymus derived

1) Memory Cells
2) Effector Cells = CD8 & CD4

CTL (CD8 + MHC I) = that kill

Helper T cells (CD4 + MHC II) = secrete cytokines that increase B cell response/antibody production & phagocytosis

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6
Q

MHC

A

presents peptide fragment to CD4/CD8 for recognition

to mature T Cell

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7
Q

MHC Restriction

A

a T cell will recognize a peptide antigen only when it is bound to a host body’s own MHC molecule

won’t recognize an MHC peptide complex that’s not the own bodies

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8
Q

T Cell Receptor (TCR)

A

heterodimer with a disulfide linked alpha & beta chain
(analogous to BCR’s Ig alpha & beta)

5 invariant polypeptide chains (3 CD3 proteins & 2 other chain - weird greek letter) = signal transduction

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9
Q

B Cell Receptor (BCR)

A

Membrane IgM or IgD & associated signal proteins Ig alpha & beta

CD21 = CR2 receptor for complement protein that promotes B Cell activation & attached to BCR
(CR2 = Type 2 Complement Receptor)

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10
Q

CD4+

“Helper” T Cells

A

Secrete cytokines that:

1) Increase B cell response/antibody production
2) Recruit macrophages for phagocytosis

Release IFN-gamma, IL-2, IL-4, IL-5

IL-2

HIV = no CD4

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11
Q

CD8+

“Cytotoxic T Lymphocytes (CTL)

A

CTL (CD8 + MHC I) = that kill

Kill cells that express foreign antigen IN THEIR CYTOPLASM

Secrete Cytokines that directly kill

VIRAL

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12
Q

Natural Killer (NK) Cells

A

Innate Immune System lymphocyte

Not variable, very general

Inhibitory or Activating:
- Inhibitory = recognized self MHC class I & tells to not attack
-default is to stay inhibitory; but then
become activated
- Activating = recognizes expressed/up-regulated on stressed/infected/DNA damaged cells -> then cells are eliminated)

Kills by tagging & then gets opsonized/phagocytosed

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13
Q

CD28

A

Cluster of Differentiation 28

Co-stimulator protein on TCR complex

Stimulatory signals required for T cell activation and survival

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14
Q

MHC

A

MHC for humans = HLA (Human Leukocyte Antigen) Complex

Chromosome 6 & HIGHLY polymorphic

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15
Q

MHC Class I

A

CD8+ Cytotoxic T Lymphocytes

HLA-A, HLA-B, HLA-C

Structure:
1 alpha chain with 3 domains
1 Beta microglobulin

Peptide in cleft is from proteins synthesized int he cytoplasm

VIRAL

longer peptide because open ends?

Binds peptides that are 8-10 AA in length

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16
Q

MHC Class II

A

CD4+ “Helper T Cell”

HLA-D
Structure: Heterodimer
1 Alpha Chain with 2 alpha domains
1 Beta Chain with 2 beta domains

Binds peptides that are 15-24 AA in length

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17
Q

B Lymphocytes

A

Memory Cells

Effector Cells = produce Antibodies

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18
Q

Dendritic Cells

A

Major APC

Interdigitating DC - lots of MHC I & costimulatory molecules to capture & present to T CELLS

Langerhans cells = Under epthelia

Follicular DC (FDC)= located in germinal centers of lymph FOLLUCLES

  • bear receptors for Fc tails of IgG & complement proteins that work to trpap antigens bound to antibodies/complement (antigen filter)
  • Then present to B CELLS
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19
Q

APC

A

Captures microbial antigens & displays them on membrane to lymphocytes

Dendritic Cells
Macrophages
B Cells -> Helper T Cells

Protein antigens are proteolytically digested & then displayed on MHC clefts

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20
Q

IgM

A

membrane bound Ig/Antibody expressed on cell’s surface

Forms the B Cell Receptor (BCR)

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21
Q

IgA

A

Secreted in mucosal tissues

Neutralizes microbes in the lumen of mucosal tissues (respirator & GI tracts)

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22
Q

IgE

A

Surface of mast cells & Eosinophils

Coats helminthic parasites & kills them

TH2 cells

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23
Q

IgD

A

expressed on the surface of B Cells

NOT secreted

24
Q

Primary/Generative Lymphoid Organ

A

Bone Marrow & Thymus

25
Secondary/Peripheral Lymphoid Organ
adaptive immune response develops & lymphocytes mature/specialize
26
IFN-gamma
ACTIVATES macrophages Released by activated macrophages & DC, endothelial cells, lymphocytes & mast cells secreted by NK cells early innate immune response activates macrophages, stimulates B cell antibody production, activates complement & coats microbes for phagocytosis
27
IL-2
Activates T Cells & tells to proliferate & differentiate Regulate lymphocyte response & effector functions in ADAPTIVE immunity Proliferation & Differentiation of lymphocytes growth factor that acts on CD4+ & stimulates proliferation
28
Helper T cell Cubsets
TH1 - Recognize antigens of microbes ingested by phagocytes & activates phagocytes to kill microbes - produce IFN-gamma (activates macrophages, stimulates B cell antibody production, activates complement & coats microbes for phagocytosis) TH2 - Activate Eosinophils - Think allergies & asthma - Produces IL-4 (stimulates B cell differentiation into IgE secreting plasma cells) - Produces IL-5 (activates eosinophils) - Produces IL-13 (activates mucosal epithelial cells to secrete mucus & expel microbes) TH17 - Enhance leukocyte recruitment & stimulate inflammation - Produces IL-17 (recruits neutrophils & promotes inflammation)
29
IL 12
early innate immune response Released by activated macrophages & DC, endothelial cells, lymphocytes & mast cells
30
IL-23
early innate immune response Released by activated macrophages & DC, endothelial cells, lymphocytes & mast cells
31
TNF-alpha
chemoattractant early innate immune response Released by activated macrophages & DC, endothelial cells, lymphocytes & mast cells
32
IL-1
chemoattractant early innate immune response Released by activated macrophages & DC, endothelial cells, lymphocytes & mast cells
33
IL-4
Regulate lymphocyte response & effector functions in ADAPTIVE immunity Proliferation & Differentiation of lymphocytes stimulates B cell differentiation into IgE secreting plasma cells
34
IL-5
activates eosinophils
35
Colony Stimulating Factor
stimulates hematopoiesis Increase output of Leukocytes from bone marrow
36
CD40 & CD40Ligand
Co-stimulatory protein on APC ( B Cells & Macrophages) CD40 & CD40 Ligand bind & activate APC
37
IL-13
Activates mucosal epithelial cells to secrete mucus & expel microbes
38
IL-17
recruits neutrophils & promotes inflammation | released by TH17
39
Affinity maturation
process of Helper T cells that stimulate the production of antibodies with higher antigen affinity refinement of antibody production
40
IL-22
a
41
TGF - Beta
a
42
IL-23
a
43
IL-6
a **GO BACK THROUGH ALL CYTOKINES***
44
IgG
Antibodies coat/opsonize microbes & target them for phagocytosis by Neutrophils & macrophages Express Fc tails Activates Complement system by Classical Pathway Stimulates by IFN-gamma & TH! cells Actively transported across placenta to create passive immuntiy
45
Immediate (Type I) Hypersensitivity
Hallmark - Production of IgE antibodies vascular permeability & smooth muscle contraction Disorders: Allergy, asthma, allergic rhinitis, conjunctivitis Hives/uticaria, Anaphylaxis, atopy ``` Mechanism: Activation of T2 helper cell & antibody class switching -> IgE ``` MEDIATORS OF TYPE I RESPONSE * CD4+ T helper cell subtype: “Th2 cell” - IL-4 promote switching of B cells from IgM to IgE production and further Th2 development - IL-5 induce expansion and activation of eosinophils - IL-13 promote switching of B cells from IgM to IgE production and stimulate mucus secretion by epithelial cells 3 groups of mediators released: Immediate: vasoactive amines released from mast cells 1) Vasoactive Amines released/degranulate (histamine, proteases, ECF/NCF) (EARLY) 2) Membrane Phospholipids/lipid mediators (AA pathway = Prostaglandins & Leukotrienes) Late Phase: cytokines/inflammatory response 3) Cytokine secretion - > immediate release from mast cells & later recruits inflammatory cells (LATE) - TNF; amplifying TH2 response Symptoms: vascular dilation, edema, smooth muscle contraction, mucus production, inflammation EOSINOPHILS - late phase *Eosinophil chemotactic factor (ECF) produced by mast cells recruit eosinophils to tissue site. *IL-5 produced by Th2 cells promote growth and activation of eosinophils. *Secrete major basic protein and eosinophil cationic protein toxic to epithelial cells *Produce leukotriene C4 and platelet activating factor (PAF) that directly activate mast cells
46
Antibody-mediated (Type II) Hypersensitivity
IgG & IgM production *Specific antibody binding to cell surface antigen results in injury to cell via variety of potential mechanisms Disorders: Autoimmune, hemolytic anemia (Fetal Rh attack), Good pasture syndrome (Table 4-3) Mechanism: 1) Opsonization/phagocytosis (Fetal Rh factor); Antibodies IgG & IgM bind to antigen on cell surface (either intrinsic (auto antigen) or exogenous (foreign) [e.g. drug] that attaches to cell surface) => 2) Complement & Fc receptor mediated inflammation (Good pasture - Kidney & lung functions) degranulation of mast cells => recruitment of leukocytes 3) Antibodies bind to ACh receptor & stimulate/block signaling (block = Myasthenia Gravis; stimulate = Graves disease/hyperthyroidism) Symptoms: variety - see Table 4-3 Phagocytosis & lysis of cells, inflammation, functional derangements without cell/tissue injury
47
Immune complex-mediated (Type III) Hypersensitivity
- Soluble antigen & free floating complex, activates complement & inflammatory cascade Disorders: - Vasculitis, lupus, glomerulonephritis, serum sickness, Arthus reaction - Lots of "-itis"es Mechanism: - Antibody binds to circulating antigens to form immune complex - Immune complexes deposit in preferred tissue sites and elicit inflammatory response: - Blood vessel wall (vasculitis) - Glomeruli (glomerulonephritis) - Joints (arthritis) - Immune complex activates complement to recruit neutrophils; mechanism of injury similar regardless of tissue site - Large IC (Immuno Complex) - rapidly cleared because so big/obstructive - Small - poorly cleared, circulate, & deposit in tissues (filters); deposit inflammatory mediators -> causing inflammation Symptoms: Abnormal & location specific Inflammation Inflammation, necrotizing vasculitis/fibrinoid necrosis
48
Cell Mediated (Type IV) Hypersensitivity
T Cells gone awry Disorders: Contact dermatitis/poison ivy, MS, DM1, TB Mechanism: - CD4+ T cells react to foreign or self-antigens, release cytokines and differentiate into: -Th1 cells (IFN-γ TNF-α); macrophage activation -Th17 cells (IL-17, IL-22): neutrophils activation - CD4+ T cells recruit CD8+ T cells [cytotoxic T lymphocytes (CTL)] 2 Types: 1) DTH = CD4 mediated S/s: Contact dermatitis 2) Cellular cytotoxicity = CD8 mediated S/s: CD8+ attacking own cells (MS = myelin sheath, DM1 = Islet cells ) * Type I diabetes mellitis: T cells react with antigens of pancreatic islet β cells (insulitis) * Multiple sclerosis: T cells react with antigens in CNS myelin (perivascular inflammation in white matter and demyelination) * Rheumatoid arthritis: T cells react with antigens in joint synovium (chronic arthritis) * Contact sensitivity: T cells react with antigens of poison ivy and poison oak (dermatitis with blisters) Symptoms: perivascular cellular infiltrates, edema, granuloma formation & cell distruction
49
Sjogren Syndrome
destroy the exocrine glands, specifically the salivary and lacrimal glands ``` xerostomia (dry mouth) keratoconjunctivitis sicca (dry eyes) ``` Primary Sjögren’s = occurs by itself Secondary Sjögren’s = another connective tissue disease is present (RA & SLE)
50
Mikulicz Syndrome
Benign enlargement of the parotid and/or lacrimal glands Sometimes, but not always, associated with Sjögren's syndrome
51
Scleroderma/Systemic Sclerosis
Characterized by thickening of the skin caused by accumulation of collagen, and by injuries to the smallest arteries Limited cutaneous scleroderma = skin on the face, hands and feet Diffuse cutaneous scleroderma = covers more of the skin, and is at risk of progressing to the visceral organs, including the kidneys, heart, lungs and gastrointestinal tract ``` CREST syndrome C = Calcinosis R = Raynaud's phenomenon E = Esophageal dysfuction S = Sclerodactyl (skin thickening) T = Telangiectasias (dialated capillaries on face, hands, mucous membranes) ```
52
Amyloidosis
amyloidosis is a non-specific term that refers to a number of different diseases Amyloids are proteins whose secondary structure changes, causing the proteins to fold in a characteristic form, the beta-pleated sheet Normally soluble proteins=> amyloids, they become insoluble and deposit in organs or tissues, disrupting normal function Congo Red => Apple green under polarized microscope ``` Systemic = more than one organ system Localized = 1 organ system/tissue type ``` ``` Primary = disordered immune cell function Secondary/Reactive = complication of some other chronic inflammatory/tissue-destroying disease ```
53
Systemic Lupus Erythematosus (SLE)
Immune system attacks healthy tissues Remissions Characteristic rash - thought to be from wolf bite ``` Systemic = Type II & III Hypersensitivity Discoid = skin lesions Drug-induced = chronic use of certain drugs Neonatal = infant from mother with SLE ```
54
Polymyositis/Dermatomyositis
Polymyositis = Inflammation of many muscles Dermatomyositis = Inflammation of muscles & skin follows after pregnancy Side effect of Statins
55
Fc Receptor
Protein that binds to antibodies and is attached to infected cells or invading pathogens Stimulates phagocytic or cytotoxic cells to destroy microbes On: B lymphocytes, follicular dendritic cells, natural killer cells, macrophages, neutrophils, eosinophils, basophils and mast cells

Pathophysiology (15 decks)

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