Immunology of Skin/Hypersensitivity Flashcards

1
Q

Characterized by the production of IgE antibodies against foreign proteins that are commonly present in the environment (e.g. pollens, animal danders, or house dust mites).

A

type I hypersensitivity

Immediate

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2
Q

5 Isotypes of Antibodies

A
IgA
IgD - naive B cells
IgE
IgG
IgM - naive B cells, pentamer
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3
Q

Which antibodies have no Fc receptors?

A

IgD - no constant receptor - never secreted

IgM - secreted, only secreted as pentamer hooked, constant region never exposed so no receptor

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4
Q

Activated B cell secretes ______ (pentamer) → class switch recombination to make _____ (3) via T cell helping

A

Activated B cell secretes IgM (pentamer) → class switch recombination to make IgA, IgG, IgE via T cell helping

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5
Q

Type I:

TH2 makes ______ → tells B cell to make ______

A

TH2 makes IL-4 → tells B cell to make IgE

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6
Q

Type I:
Plasma cells make ______ → bump into granulocytes which have Fc _______ receptor, bind
Antigen recognized by ______ Ab on granulocyte

A

Plasma cells make IgE → bump into granulocytes which have Fc epsilon receptor, bind
Antigen recognized by IgE Ab on granulocyte

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7
Q

Most allergens are ______

A

proteins, soluble, various functions

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8
Q

IgE production is dependent on Th____ cells and that any priming that generates a Th____ response will inhibit IgE production.

A

IgE production is dependent on Th2 cells and that any priming that generates a Th1 response will inhibit IgE production.

Type I

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9
Q

The main cytokines that are specifically relevant to a Th1 response include:
_____ produced by macrophages
_____ produced by T cells

A

The main cytokines that are specifically relevant to a Th1 response include:
interleukin-12 (IL-12) produced by macrophages
IFNγ produced by T cells

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10
Q

By contrast, the primary cytokines relevant to a Th2 response are:
____
____
_____

A

By contrast, the primary cytokines relevant to a Th2 response are:
IL-4 / IL13
IL-5
IL-10

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11
Q

Hyposensitization

A

Treatment to increase tolerance
drive response from Th2 to Treg to decrease response
NOT IL-4

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12
Q

Occurs when IgG or IgM antibodies are produced against surface antigens on cells of the body. These antibodies can trigger reactions either by activating complement (e.g. autoimmune hemolytic anemia) or by facilitating the binding of natural killer cells.

A

Antibody-mediated (Type II Hypersensitivity)

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13
Q

Involve the formation of immune complexes in the circulation that are not adequately cleared by macrophages or other cells of the reticuloendothelial system. The formation of immune complexes requires significant quantities of antibody and antigen. The classical diseases of this group are systemic lupus erythematosus (SLE), glomerulonephritis, and serum sickness

A

Immune Complex (Type III)

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14
Q

Arthus reaction

A

Rash at site of drug injection (2nd injection)
1st inj - prime immune response, activate T cells, B cells → make Ab, memory response → massive inflammation at second injection

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15
Q

3 variants of Type IV hypersensitivity

A

There are three variants of type IV hypersensitivity reaction – contact, tuberculin, and granulomatous.

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16
Q

Examples of Cell Mediated Hyper.

A
contact sensitivity (e.g. to nickel or plants such as poison ivy)
the delayed hypersensitivity responses of leprosy or tuberculosis
the exaggerated response to viral infections such as measles
the persistent symptoms of allergic disease (i.e. later constriction in asthma - first is immediate)
17
Q

occurs at the site of contact with an allergen. Sensitization occurs when skin dendritic cells internalize and process epicutaneously applied hapten and migrate to the draining lymph nodes where they activate antigen-specific T cells. On re-exposure to antigen, cytokines produced by skin cells (e.g. keratinocytes, Langerhans’ cells), recruit antigen-specific, and also non-specific T cells, and macrophages.

A

Contact hypersensitivity (type IV)

18
Q

induced by CD4 T cell responses to soluble antigens from a variety of organisms. It is useful as a diagnostic test to detect infection with a number of infectious agents

A

tuberculin-type hypersensitivity (type IV)

19
Q

clinically the most important form of type IV hypersensitivity.
Persistence of antigen leads to chronic T cell activation, differentiation of macrophages into epithelioid cells, and their fusion to form giant cells → tissue pathology.

A

Granulomatous hypersensitivity (type IV)

20
Q

_______ is driven by T cell activation of macrophages, and is dependent on TNF. Inhibition of TNF leads to breakdown in _______.

A

Granuloma formation is driven by T cell activation of macrophages, and is dependent on TNF. Inhibition of TNF leads to breakdown in granulomas.

21
Q

Small molecule can elicit immune response, complex with other proteins (ie. skin) = carrier molecule to antagonize immune system

A

Hapten (type IV)

22
Q

IgG antibodies can trigger reactions either by _____ or by facilitating the binding of _______

Type ____ Hypersensitivity

A

IgG antibodies can trigger reactions either by activating complement (e.g. autoimmune hemolytic anemia) or by facilitating the binding of natural killer cells.

Type II - antibody mediated

23
Q

Type I hallmarks

A

IgE mediated - Immediate

Systemic anaphylaxis + localized anaphylaxis (hayfever, asthma, hives, food allergies, eczema)

24
Q

type 2 hallmarks

A

IgG mediated - Ab-mediated
via complement/natural killer cells

Blood transfusions, AI hemolytic anemia, erythroblastosis fetalis

25
Q

Type 3 hallmarks

A

Immune complex mediated
Need a lot of Ag-Ab

SLE, necrotizing vasculitis, RA, serum sickness

26
Q

Type IV hallmarks

A

Cell mediated
TH1 and THC cells

Contact dermatitis, tubercular lesions, or graft rejection (also crohn’s, granulomas)