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SFM Exam 2 > Shnyra- Hypersensitivity > Flashcards

Shnyra- Hypersensitivity Flashcards

1
Q

What mediates Type I hypersensitivity responses?

A

IgE. They result from the actions of mediators secreted by mast cells

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2
Q

What mediates Type II hypersensitivity responses?

A

IgG & IgM that bind tissues Ags & cause complement-dependent tissue injury/disease

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3
Q

What mediates Type III hypersensitivity responses?

A

Circulating Ag-Ab complexes which deposit in vessel walls & cause complement dependent injury in vessel walls

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4
Q

What mediates Type IV hypersensitivity responses?

A

T cells & results from inflammation caused by cytokines produced by CD4+ Th1 cells, Th17 cells, and macrophage or killing host cells by CD8+ CTLs

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5
Q

Define atopy

A

A genetic tendency to develop allergic diseases/allergic rxns

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6
Q

What do the effects of histamine, prostaglandins & leukotrienes combined induce?

A

Increases in BP & permeability

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7
Q

What causes edema?

A

Increased movement of fluid from the intravascular to the interstitial space

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8
Q

In the mechanism of edema, how are leukotrienes and histamine different?

A

Leuko-drain larger venules (vasoconstriction)

Histamine- post cap venules (vasodilation)

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9
Q

Before clinical presentation, what is occurring in the process of immediate hypersensitivity?

A

Activation of Th2 cells by first exposure to allergens & generation of plasma cells which produce IgE, IgE bind to FceR1 receptors on mast cells

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10
Q

What are late phase Type I hypersensitivity rxns characterized by?

A

Inflammatory infiltrate rich in eosinophils, neutrophils, & T cells

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11
Q

What are the 4 purposes of Allergen Specific Immunotherapy?

A
  1. induce peripheral T cell tolerance
  2. Increase thresholds for mast cell & basophil activation by allergens
  3. to decrease IgE-mediated histamine release by mast cells
  4. to generate allergen-specific inducible FOXP3+ CD4+ CD25+ Treg cells
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12
Q

In terms of allergen desensitization, define immune deviation

A

Repeated exposure to desensitizing allergen induces a shift from Th2 to Th1 CD4 cells that results in the generation of cytokines (IFN-y) which inhibit IgE production

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13
Q

Explain Type II Hypersensitivity

A

IgG can opsonize cells that leads to phagocytosis of the cells through FcyR or CR1 receptors. Neutros and macros that are activated in this manner release their inflammatory mediators (ROS & lysosomal enzymes damage the adjacent tissues & cause inflammation)
IgM and IgG can act. classical pathway which produces C5a and C3a which promote leukocyte recruitment & inflammation

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14
Q

What do Ab-dependent effector mechanisms of Type II Hypersensitivity require?

A

Immune cells expressing Fcy receptor type III (FcyRIII) on their surface & target cells coated with Ab recognizing ags on the cell surface
NK cells express high levels of FcyRIII & are regarded as the key players in this process

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15
Q

What is myasthenia graves?

A

Inhibiting of the binding of acetylcholine neurotransmitter to the ACh receptor that causes autoimmunity

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16
Q

Define immune-complex anemias

A

Abs form immune complexes with a drug. the ICs can bind to the erythrocyte surface via CR1. Complement is activated on RBC surface which causes hemolysis

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17
Q

Define autoimmune anemias

A

Drug induces anti-drug Abs that cross react with an Rh Ag on RBCs. Ab binding to Rh Ag activates phagocytosis & complement. Treatment may require immunosuppression or removal of ICs by plasmapheresis

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18
Q

What is serum sickness (Type III hypersensitivity)?

A

Can be induced by IV administration of a protein Ag to a previously immunized patient that leads to formation of IC and systemic vasculitis

19
Q

What is arthus rxn (Type III hypersensitivity)?

A

Induced by subcutaneous administration of a protein Ag to a previously immunized animal. Ag causes local formation of ICs at the site of AG injection that leads to local vasculitis (compare to the systemic vasculitis in serum sickness)

20
Q

What 3 things trigger a Type IV hypersensitivity reaction?

A

Autoimmunity
Persistent responses to environmental Ags
Microbial Ags

21
Q

How long does it take a Type IV hypersensitivity rxn to occur & what is it mediated by?

A

24-48 hours & it is mediated by Ag-activated CD4+ T cells, CD8+ T cells, and macrophages which release mediators

22
Q

What is central tolerance?

A

Induced by immature self-reactive lymphocytes in the primary lymphoid organs. Ensures that mature lymphocytes are not reactive to self Ags

23
Q

What is peripheral tolerance?

A

Induced in mature self-reactive lymphocytes in peripheral sites. Prevents activation of these potentially dangerous lymphocytes in the tissues

24
Q

In terms of central tolerance, what is positive selection?

A

Thymocytes that bind self-Ags below a certain threshold are positively selected & are allowed to migrate into the periphery as mature T cells

25
Q

In terms of central tolerance, what is negative selection?

A

Thymocytes which strongly bind self-Ags undergo negative selection & are deleted by apoptosis
In some cases, strong binding of self-Ags leads to activation of FoxP3 gene & production of natural Treg cells (nTreg cells)

26
Q

What is a critical factor for survival & functional competence of nTreg cells?

A

IL-2

27
Q

What is RORyt and how is it induced?

A

It is induced by IL-6 and IL-1 in combination with TGF-B. It is a major transcription factor driving differentiation of Th17 cells which are important in autoimmunity

28
Q

What do IL-10 & TGF-B inhibit?

A

Proliferation & effector functions of T cells, activation of M1 macrophages, differentiation of Th1 cells

29
Q

What does TGF-B regulate/stimulate?

A

Regulates differentiation of induced FoxP3+ Treg cells

stimulates production of IgA in inducing B cells to switch to this isotype. Stimulates collagen synthesis by fibroblasts

30
Q

Explain the importance of anti-CTLA4 & anti-PD1 Abs.

A

Used for treatment of cancer pts. Enhance antitumor immune responses & tumor regression. Side effect: may lead to autoimmune diseases

31
Q

What leads to anergic cells?

A

Ag recognition without adequate CD80:CD28 costimulation induces anergy. Anergic cells survive but are incapable of responding to Ags

32
Q

What two major mechanisms eliminate autoreactive B cells in central tolerance?

A

Anergy & clonal deletion

33
Q

What is the purpose of BCR editing in Central B cell tolerance?

A

Leads to the repeated rearrangement & replacement of the genes that encode Ig Light chain until BCRs which do not recognize self-Ags are produced or the cell dies

34
Q

What is CD22’s role in peripheral B cell tolerance?

A

It is an inhibitory coreceptor. When act., it recruits SHP-1 tyrosine phosphatase that attenuates BCR signaling. It is involved in B cell tolerance to self-Ags

35
Q

What happens to cellular debris in pts with complement C1, C2, and C4 deficiencies?

A

It is NOT removed from circulation but instead stimulates the production of autoantibodies

36
Q

What is the role of CTLA-4 in peripheral tolerance?

A

Inhibitory receptor. Provides signals that terminate immune responses. Prevents activation of autoreactive T cells & maintains self-tolerance in healthy pts. It may lead to a break of self-tolerance & the development of autoimmunity

37
Q

What happens in CTLA-4 KO mice?

A

Uncontrolled lymphocyte activation with massively enlarged LNs & Spleen associated with FATAL multi-organ lymphocytic infiltrates. Blocking of CTLA-4 w/anti-CTLA-4 worsens the ongoing autoimmune diseases in animal models

38
Q

What is Fas/FasL signaling?

A

Recognition of self-Ags may lead to expression of death receptors (fas) & its ligand (FasL) on T lymphocytes. Fas engagement leads to apoptosis of the cells by the death receptor (Extrinsic) pathway. Defects in Fas-FasL signaling result in autoimmune lymphoproliferative syndrome (ALPS)

39
Q

What causes epitope spreading?

A

An immune response to secondary epitopes which are distinct from the primary disease causing epitope

40
Q

What is the principal SLE diagnostic test?

A

The presence of anti-nuclear Abs

41
Q

What are the principal immune cells involved in Rheumatoid Arthritis?

A

Th1, Th17, activated B cells, M1 macrophages

42
Q

What cells can trigger an inflammatory response in the white matter of the brain?

A

TNF-a, IL-6, IL-17, TGF-B, IFN-y

43
Q

What occurs in multiple sclerosis?

A

Development of plaques in the white matter by stripping myelin from neurons. Popular treatment= cytokine IFN-B that attenuates the action of the proinflammatory cytokines

44
Q

What happens in the immunopatheogenesis of T1D?

A

Local APCs present Ags in the context of Class II MHC molecules & secret IL-12 that plays an important role in the pathogenesis of T1D. APCs activate Ag-specific CD4+ Th1 cells which produce IFN-y. IFN-y inhibits Th2 cytokines production (IL-4, 5, 10) & enhances IL-1b, TNF-a, ROS production by macrophages which all are toxic to islet beta cells

SFM Exam 2 (7 decks)

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