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TERM 3- Postmidterm > L47, L49- Hypersensitivity, Immune Tolerance, Autoimmunity > Flashcards

L47, L49- Hypersensitivity, Immune Tolerance, Autoimmunity Flashcards

1
Q

Type I hypersensitivity reactions have (1) as the immune reactant and Ag in the (2) form. (1)-(2) complex binds to (3) on (4) cells inducing (5).

A 
1- IgE
2- soluble
3- FcεRI
4- mast cells (basophils, eosinophils)
5- degranulation of mast cells
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2
Q

Type II hypersensitivity reactions have (1) as the immune reactant and Ag in the (2) form. (1) binds to (3) leading to (4) activation and (5) of target cell.

A 
1- IgG or IgM
2- cell-bound
3- cellular Ag
4- complement (classical pathway)
5- lysis
(Note- IgG can lead to ADCC w/ Tc / NK cells, macrophages, neutrophils)
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3
Q

Type III hypersensitivity reactions have (1) as the immune reactant and Ag in the (2) form. (1)-(2) complexes are deposited in tissues which activates (3) resulting in (4) and recruitment of (5) which will cause local tissue damage.

A 
1- IgG & IgM
2- soluble (SERUM)
3- complement
4- inflammation (C3a, C5a)
5- neutrophils (release enzymes => tissue damage)
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4
Q

Type IV hypersensitivity reactions have (1) as the immune reactant and Ag in the (2) form. (1) secretes (3) to activate (4) cells.

A

1- T cells (Th1)
2- soluble or cell-bound
3- CKs
4- macrophages & Tc cells

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5
Q

hypersensitivities take place in response to… (hint- 3 things)

A
  • infection that can’t be cleared
  • normally harmless exogenous substance (allergen)
  • auto-antigen
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6
Q

define hypersensitivity

A

exaggerated or inappropriate immune response => tissue damage

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7
Q

Type _ hypersensitivity(ies) is(are) Ab mediated (humoral)

Type _ hypersensitivity(ies) is(are) cell mediated

A

I, II, III –> Ab mediated

IV –> cell mediated

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8
Q

(T/F) hypersensitivities occur upon first contact with Ag

A

F- never, sensitization occurs on 1st contact, hypersensitivity always upon re-exposure

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9
Q

define atopy

A

genetic predisposition to produce IgE in response to many common, naturally occuring Ag/allergens (~20% individuals in US)

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10
Q

IgE is the usual response against (1), where it binds (2) after binding Ag on (3) cells

A

1- metazoal parasites (too large to be phagocytized)
2- FcεRI (high-affinity)
3- mast cells, basophils (+ eosinophils)

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11
Q

Type I hypersensitivities are (immediate/delayed) reactions

A

immediate-type hypersensitivity

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12
Q

describe development of IgE against (harmless) Ags in upon first contact

A
  • IgM on B cell binds Ag
  • Th2 cell binds B cell via CD4 and releases IL-4 / IL-13
  • ILs stimulate class switching to IgE
  • results in memory B cell + plasma cell producing Allergen specific IgE
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13
Q

list the primary mediators in mast cell granules

A

(made before and stored)

histamine, proteases, eosinophil chemotactic factor, heparin

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14
Q

list the secondary mediators in mast cells

A

(2-4 hrs after immediate response)

platelet-activating factor, LTs, PGs, bradykinins, some CKs + chemokines

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15
Q

compare atopic to immune allergy response

A

(based on genetic + environmental factors)
-Atopic: Th2, IgE; not exposed to pathogens regularly (urban enviro., western diet, widespread Antibiotic use)

-Immune: Th1, IgG, exposed to pathogens regularly (hygiene hypothesis)

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16
Q

examples of localized and systemic Type I hypersensitivity

A

Local: allergic rhinitis, asthma, food allergies, wheals, atopic eczema

Systemic: anaphylaxis

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17
Q

explains desensitization using Abs

A
  • for type I hypersensitivity in people with mild to moderate allergies (not for extreme- must have some tolerance)
  • development of IgG as ‘blocking Abs’ preventing IgE binding and rxn with mast cell
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18
Q

Type II hypersensitivity can involve cytotoxic process where (1) is activated, phagocytosis occurs via (2) receptor, and (3) occurs via NK cells and eosinophils. Non-cytotoxic process involves (4).

A

1- classical complement pathway (IgG, IgM)
2- FcR and complement receptors
3- ADCC (Ab-dep. cellular cytotoxicity)
4- interference with receptors (anti-receptor Abs)

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19
Q

Autoimmune hemlytic anemia (HDNB) is considered a type (1) hypersensitivity. It involves (2) Ag, has (3) as a mechanism leading to (4) as clinical manifestations.

A

1- type II (cytotoxic)
2- RBC membrane proteins (Rh, ABO)
3- opsonization, phagocytosis, complement-mediated destruction of RBCs
4- hemolysis, anemia

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20
Q

Acute rheumatic fever is considered a type (1) hypersensitivity. It involves (2) Ag, has (3) as a mechanism leading to (4) as clinical manifestations.

A

1- type II (cytotoxic)
2- streptococcal cell-wall Ag (cross-reaction with myocardial Ag)
3- inflammation + macrophage activation
4- myocarditis, arthritis

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21
Q

Goodpasture syndrome is considered a type (1) hypersensitivity. It involves (2) Ag, has (3) as a mechanism leading to (4) as clinical manifestations.

A

1- type II (cytotoxic)
2- type IV collagen (BM of kidney glomeruli + lung alveoli)
3- complement + Fc-receptor-mediated inflammation (IgG accumulation in tissue)
4- nephritis, lung hemorrhage, linear Ab deposits

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22
Q

Myasthenia Gravis is considered a type (1) hypersensitivity. It involves (2) Ag, has (3) as a mechanism leading to (4) as clinical manifestations.

A

1- type II (non-cytotoxic)
2- AChR
3- blocks ACh binding
4- muscle weakness, paralysis

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23
Q

Graves disease is considered a type (1) hypersensitivity. It involves (2) Ag, has (3) as a mechanism leading to (4) as clinical manifestations)

A

1- type II (non-cytotoxic)
2- TSH receptor
3- stimulates TSH receptor
4- hyperthyroidism (followed by hypothyroidism)

24
Q

describe Erythroblastosis fetalis

A
  • Rh+ fetus, Rh- mother
  • upon 1st vaginal birth, mother exposed to Rh –> develops IgG against
  • upon 2nd pregnancy –> IgGs can cross placenta and damage fetus
  • RhoGAM administered to block Rh from being exposed to mother
25
Q

describe Arthrus reaction

A

(type III hypersensitivity)

  • individual sensitized to Ag
  • Ag administered locally (SQ, ID)
  • rxn occurs locally
  • mast cell mediated
26
Q

what is serum sickness

A

(type III hypersensitivity)

  • response to foreign protein after receiving anti-serum, which is usually from another animal containing anti-toxin
  • deposition of serum immune complex (Ag-IgG/IgM) systemically
  • fever, vasculitis, arthitis, nephritis
27
Q

Type IV hypersensitivities are (immediate/delayed) reactions

A

delayed-type hypersensitivity (48-72 hrs after second exposure)

28
Q

Type I hypersensitivities are important for the clearance of…

A
  • intracellular pathogens (ex. M. tuberculosis, Leishmania major)
  • if Ag persists –> lytic products of macrophages can damage healthy tissue
29
Q

describe sensitization phase of Type IV hypersensitivity

A

upon first exposure, APCs (macrophages, Langerhans cells) present Ag to naive T cells generating Th1 (generally)

30
Q

describe effector phase of Type IV hypersensitivity

A
  • Th1 cells secrete CKs and chemokines to effect macrophages

- macrophages inc MHC-II, TNF receptors, O2 radicals + NO

31
Q

prolonged DTH can lead to formation of….

A

(delayed-type hypersensitivity)

granuloma (surrounding resistant intracellular microbe)

32
Q

define central tolerance

A
  • deleting T or B clones before maturity if they have receptors that recognize self-Ags with great affinity
  • ‘negative selection’
  • occurs in primary lymphoid tissues
33
Q

define peripheral tolerance

A
  • killing lymphocytes that bind self-Ag (high dose) in secondary lymphoid tissue
  • regulated by apoptosis or anergy (no proliferation)
34
Q

(T/F) B cells can escape anergy or deletion in peripheral tolerance

A

T- Receptor Editing can occur; further rearrangement of their immunoglobulin genes

35
Q

in peripheral tolerance (1) cells may be responsible for controlling this process, as they recognize (2) and then will (3)

A

1- Treg cells (CD4+)
2- self-Ag (intermediate affinity)
3- suppress T cells (non-reg) that bind with low affinity to self-Ag

36
Q

list the 5 ways immunogens can become tolerogens

A
  • high doses of Ag
  • persistent Ag
  • IV / oral introduction
  • absent adjuvants
  • low levels of co-stimulators: CD28/B7 low => CTLA-4 binding B7 to inhibit
37
Q

(T/F) CD28 has higher affinity for B7 than CTLA-4

A

F- CTLA-4 (inhibitory) has higher affinity than CD28 (activator)

38
Q

tolerogens induce ______ in mature lymphocytes

A

apoptosis or anergy

39
Q

how does the body prevent autoimmunity

A
  • central tolerance
  • peripheral tolerance
  • immune regulation (Treg cells)
40
Q

list the immunologically privileged sites and what occurs there (include the CK that might be most responsible)

A
  • brain, eyes, testis, placenta (only exposed to immune system in trauma)
  • T cells enter => undergo apoptosis
  • foreign Ags (+ tissue grafts) don’t elicit immune responses
  • tolerance&raquo_space; destructive reponse
  • TGF-β may be key CK responsible
41
Q

list the 4 ways peripheral tolerance prevents autoimmunity

A
  • lack of co-stimulatory
  • lack of Ag presentation
  • negative feedback prevents overstimulation
  • T cells entering immune-privileged sites undergo apoptosis
42
Q

list the 6 discussed causes of autoimmunity

A
  • Tolerance => thymic breakdown (genetic) OR in periphery (enviroment)
  • HLA (human leukocyte Ag) = genetic predisposition
  • release of sequestered Ags (tissue traumas)
  • Infection => mimicry of self-Ags (short-lived and reversible)
  • some viruses activate B cells non-specifically
  • inappropriate MHC expression
43
Q

(T/F) autoimmune diseases affect women more than men

A

T

44
Q

which hypersensitivity mechanisms can result in autoimmunity

A
  • Type II, Ab mediates, immediate rxn
  • Type III, immune complex mediated
  • Type IV, cell-mediated, delayed rxn
45
Q

Autoimmune thrombocytopenia purpura is considered a type (1) hypersensitivity. It involves (2) Ag, has (3) as a mechanism leading

A

1- type II (cytotoxic)
2- platelets’ integrin or glycoprotein
3- Abs destroy platelets => thrombocytopenia

46
Q

list the 3 autoimmune anemias (include Ags and through what hypersensitivity mechanism)

A

[type II cytotoxic mechanism]

  • hemolytic anemia: Abs for Rh or AB(O) RBCs
  • drug induced anemia
  • pernicious anemia: Ab against intestinal protein responsible for B12 uptake
47
Q

Pernicious anemia is considered a type (1) hypersensitivity. It involves (2) Ag, has (3) as a mechanism leading to (4) as clinical manifestations.

A

1- type II (cytotoxic)
2- intestinal B12 protein responsible for uptake
3- no B12 absorption from intestine
4- anemia (+ neurological symptoms)

48
Q

systemic autoimmunities are usually due to type ___ hypersensitivity mechanisms

A

type III (immune complex mediated)

49
Q

Systemic Lupus Erythematous is considered a type (1) hypersensitivity. It involves (2) Ag, has (3) as a mechanism leading to (4) as clinical manifestations.

A

1- type III
2- antinuclear Ags (ANA): dsDNA (mainly), histones, platelets, leukocytes, clotting factors
3- excessive complement activation (systemically)
4- fever, weakness, arthritis, rash, kidney issues
(note typically affects middle aged women most)

50
Q

what is an ANA and how is it detected

A
  • antinuclear Ag: dsDNA, histone, ect.

- detected via indirect immunoflorescent Ags

51
Q

Polymyositis is considered a type (1) hypersensitivity. It involves (2) as target Ag.

A

1- type IV

2- muscle cells

52
Q

Hasimoto’s Thyroiditis is considered a type (1) hypersensitivity. It involves (2) Ag, has (3) as a mechanism leading to (4) as clinical manifestations.

A

1- type IV
2- thyroid Ags- mainly TPO (thyroid peroxidase)
3- destruction of thyroid tissue + accumulation of incomplete thyroid hormone
4- hypothyroidism, goiter
(mainly affects middle aged women)

53
Q

Insulin dependent DM (type I) is considered a type (1) hypersensitivity. It involves (2) Ag, has (3) as a mechanism leading to (4) as clinical manifestations.

A

1- type IV
2- β-cell (pancreas) elements
3- Abs / T cells destroy insulin producing β-cells
4- diabetes

54
Q

Multiple sclerosis is considered a type (1) hypersensitivity. It involves (2) as a mechanism leading to (3) as clinical manifestations.

A

1- type IV
2- inflammatory lesions in myelin sheath caused by T cells
3- numbness, paralysis, vision loss

55
Q

Rheumatoid arthritis is considered a type (1) hypersensitivity. It involves (2) Ag, has (3) as a mechanism leading to (4) as clinical manifestations.

A

1- type IV
2- Fc region of IgG
3- immune complexes (T cells + IgG) depositing systemically in tissue
4- chronic inflammation of joints

56
Q

CTLA-4 is expressed on (1) cells in (2) fashion and (3) cells in (4) fashion. CTLA-4 binds to (5). Variants of CTLA-4 has been associated with the following autoimmune diseases: (6).

A

1/2- Treg cells, constitutively
3/4- activated T cells, only when activated
5- B7-1/CD80, B7-2/CD86
6- type I DM, Grave’s, Hashimoto’s. Celiac’s, SLE, others

TERM 3- Postmidterm (11 decks)

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