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H&D > Wk 2 TBL 2 Type I Hypersensitivity > Flashcards

Wk 2 TBL 2 Type I Hypersensitivity Flashcards

1
Q

What are 2 types of tolerance with regards to the adaptive immune system?

A
  1. Central - occurs in thymus
  2. Peripheral - circulating T cells
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2
Q

How does central tolerance manifest?

A

In thymus, negative selection of self-reactive T cells - undergo apoptosis OR some develop into Treg cells

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3
Q

How does peripheral tolerance manifest?

A
  1. Circulating T cells: Activated DCs (signal 1+signal 2) -> T cell activation
  2. W/o inflammation, immature DCs can generate signal 1 but no signal 2 w/ T cells -> either T cell death or anergy
  3. Tregs- convert activated DCs into regulatory DCs
    -secrete immunosuppressive cytokines (IL-10, TGFbeta)
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4
Q

What is anergy?

A

Fxnal state in which T cell has lost ability to respond to T cell receptor signals

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5
Q

Central vs peripheral tolerance

A

Central tolerance mechanisms eliminate self-reactive lymphocytes during their initial development in the bone marrow and thymus.
Peripheral tolerance mechanisms eliminate self-reactive lymphocytes that escape the radar of central mechanisms; in the peripheral tissues and secondary lymphoid organs.

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6
Q

Where do Tregs develop?

A

thymus
-to suppress autoimmune responses
-constantly circulating

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7
Q

When are Tregs induced?

A

During immune responses (to suppress immunopathology)
-also constantly circulating

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8
Q

What regulates Tregs?

A

FoxP3, a transcription factor, expressed by tTregs and pTregs

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9
Q

What happens w/ FoxP3 mutations?

A

can lead to IPEX (immunodysregulation polyendocrinopathy enteropathy X-linked syndrome)
-autoimmune disease in endocrine organs
-complete loss of fxn of FoxP3 not observed, but -> overwhelming autoimmunity and death in experimental animals

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10
Q

What is IPEX?

A

=immunodysregulation polyendocrinopathy enteropathy X-linked syndrome
-autoimmune disease in endocrine organs
-complete loss of fxn of FoxP3 not observed, but -> overwhelming autoimmunity and death in experimental animals

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11
Q

Define hypersensitivty reactions

A

=immune responses that damage human tissues
-tolerance systems don’t fxn well

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12
Q

When do hypersensitivty reactions occur?

A
  1. Response to foreign antigen (ie. Penicillin covalently attaches to surface of RBCs. penicillin-specific antibodies can develop and cause destruction of RBCs)
  2. Response to self antigen (autoimmunity) - ie RBC-specific antibody (self antigen)
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12
Q

When do hypersensitivty reactions occur?

A
  1. Response to foreign antigen (ie. Penicillin covalently attaches to surface of RBCs. penicillin-specific antibodies can develop and cause destruction of RBCs)
  2. Response to self antigen (autoimmunity) - ie RBC-specific antibody (self antigen)
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13
Q

What are the 4 types of hypersensitivity reactions?

A
  1. Type I - mediated by IgE on mast cells (ie allergic reactions)
  2. Type II -mediated by IgG (cell-associated antigens)
  3. Type III - mediated by IgG:antigen immune complexes - can be specific for autoantigens or foreign antigens
  4. Type IV - mediated by T cells (T helper cells that secrete cytokines like IFN gamma, TNF OR CTLs)
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14
Q

Why do tolerance mechanisms break down? AKA why do we get hypersensitivity reactions?

A
  1. genetics - HLA, sex, genes associated w/ immune regulation
  2. Environmental factors (smoking, weight, age, diet, etc)
  3. Infectious history (similarity b/w foreign and self antigens = molecular mimicry, which can -> destruction of self tissues)
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15
Q

How are autoimmune diseases inherited?

A

Most have complex inheritance w/ multiple loci and variable penetrance

Some driven by single gene, usually ones centrally involved in immune tolerance: CTLA-4, PD-1, Fas, FoxP3, AIRE

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16
Q

What locus is most strongly linked to autoimmune diseases?

A

HLA
MHC Class II

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16
Q

What locus is most strongly linked to autoimmune diseases?

A

HLA
MHC Class II

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17
Q

What locus is most strongly linked to autoimmune diseases?

A

HLA
MHC Class II

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18
Q

What diseases is HLA-B27 linked to?

A

Ankylosing spondylitis
Psoriasis
IBD
Reactive Arthritis

-strong contributor to relative risk and used as a diagnostic

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19
Q

What are some autoimmune consequences of infections?

A

Rheumatic fever (carditis, polyarthritis)
Reactive arthritis
Chronic arthritis in Lyme disease
Type I diabetes

-can -> molucular mimicry and autoimmune responses

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20
Q

What demographic is more susceptible to many autoimmune diseases?

A

Females
-onset often begins in 3rd, 4th or 5th decade of life
-poorly understood

21
Q

Summary

A
22
Q

What cells drive type I hypersensitivity?

A

Th2 cells

23
Q

What defines allergens?

A
  1. usually inert (non-immunogenic)
  2. inhaled: pollen, dander, mold
  3. injected: insect venom
  4. ingested: shellfish, nuts
  5. skin: latex
24
Q

How does a type I hypersensitivity reaction occur?

A

If T cell gets activated by allergen epitopes in the presence of IL-4, it induces a Th2 response
-some genetic susceptibility
-occurs during first sensitizing exposore to an allergen
-mast cells get “armed” with allergen-specific IgE

25
Q

What antibodies is activated?

A

IgE on mast cells

26
Q

What is the role of IL-4 in type I hypersensitivity?

A

Induces class switching of B cells to IgE
-> IgE-secreting plasma cells

27
Q

What do the IgE antibodies do after formation?

A

Bind to mast cells that express the Fc epsilon receptor -> mast cells become coated w/ allergen-specific IgE

28
Q

What other cytokines do Th2 cells make?

A

IL-4
IL-5
IL-10

29
Q

What does IL-5 do?

A

activates eosinophils

30
Q

What do eosinophils do in allergic response?

A

Release prostagladins, cytokines

31
Q

What happens on second exposure?

A

-mast cell can crosslink antibodies on surface -> degranulation mediated by IgE-> release of histamine, leukotrienes and proteases (enhance inflammation during tissue invasion)

32
Q

What is the role of histamine?

A

acts in the early phase allergic reaction (w/in minutes of 2nd exposure)
-induces vasodilation, allowing fluid and cells to escape into tissues -> edema, urticaria, and rhinitis
-induces bronchoconstriction -> asthmatic reaction

33
Q

What is early phase allergic reaction AKA?

A

immediate hypersensitivity

34
Q

When is late phase allergic reaction?

A

8-12 hrs after initial allergen exposure

35
Q

What mediates a late phase allergic reaction?

A

leukotrienes
cytokines: IL-4, IL-5, TNF produced by mast cells
-cytokines activate Th2, eosinophils, basophils, and neutrophils

36
Q

What are leukotrienes?

A

vasoactive lipids derived from arachadonic acid
-induce vasodilation, bronchoconstriction, and activation of many cell types (Th2, basophil, eosinophils, neutrophils)

37
Q

What is anaphylaxis?

A

Usually occurs w/ a high dose of allergens via injection (ie. bee venom) or ingested (ie peanuts, shellfish)
-> systemic effects: vasodilation, bronchoconstriction, edema, urticaria, GI distress
can -> drop in BP, poor organ perfusion, shock, eventually organ failure, death

38
Q

What is the tx for anaphylaxis?

A

Epi

39
Q

Type I hypersensitivity tx

A
  1. epinephrine
  2. anti-histamines
  3. albuterol
  4. corticosteroids
40
Q

What are the actions of epinephrine?

A

increase vasoconstriction
increase ventricular contraction
-> increase HR, BP

41
Q

What are the actions of anti-histamines?

A
  1. vasoconstriction
  2. bronchodilation
42
Q

What is the action of albuterol?

A
  1. -> bronchodilation
  2. inhibits mast cell activation

for asthmatic reactions
-is a beta-2 adrenergic receptor agonist

43
Q

Actionsof corticosteroids?

A

Non-specific immunosuppression

nasal spray
allergic rhinitis

44
Q

Summary

A
45
Q

What is tryptase?

A

the most abundant protein component of mast cell secretory granules
-basophils also produce a small amount

-used as a diagnostic marker

45
Q

What is tryptase?

A

the most abundant protein component of mast cell secretory granules
-basophils also produce a small amount

-used as a diagnostic marker

46
Q

What is allergic rhinitis?

A

-Pollens, grasses, dust mites, etc
-> increased mucus secretion, inflammation of upper airways and sinuses, urticaria, and eczema
Tx: anti-histamines, desensitization, anti-IgE antibodies, Cromolyn

47
Q

What is desensitization?

A

repeated administration of low doses of antigen to induce tolerance

48
Q

What is Cromolyn

A

drug that inhibits mast cell degranulation

49
Q

Asthma

A

=smooth muscle hyper-reactivity w/ inflammation and tissues injury caused by late-phase reaction

Tx: glucocorticoids to reduce inflammation, leukotriene antagonists and phosphodiesterase inhibitors to relax bronchial smooth muscle
-albuterol

50
Q

How is anaphylaxis diagnosed?

A
  1. rapid onset of symptoms involving skin or mucosa
  2. respiratory compromise (dyspnea, wheeze/bronchospasm, stridor, reduced peak expiratory flow, hypoxemia)
  3. reduced BP or associated symptoms and signs of end-organ malperfusions (hypotonia (collapse), syncope, incontinence
  4. persistent GI sx (crampy abd pain, vomiting)

-can be biphasic w/ recurrence of symptoms w/in 12 hrs w/o additional exposire to causative agent

H&D (23 decks)

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