Immunology review and Hypersensitivity reactions Flashcards

1
Q

Humoral immunity

A

Protects against extracellular microbes and toxins.

Part of adaptive immune system.

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2
Q

Intracellular immunity

A

Protects against intracellular microbes and tumor cells.

Part of adaptive immune system.

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3
Q

Generative lymphoid organs (primary or central)

A

sites where T and B lymphocytes mature and become competent to respond to antigens (thymus for T lymphocytes, bone marrow for B lymphocytes)

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4
Q

Peripheral lymphoid organs (secondary)

A

Sites where the adaptive immune response is initiated (lymph nodes, spleen, mucosal and cutaneous lymphoid tissues (GI tract, respiratory tract, skin).

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5
Q

Reactive follicular hyperplasia

A
  • Germinal center develops in follicle and becomes hyperplastic
  • Occurs when B lymphocytes respond to an antigen.
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6
Q

MHC function

A

The physiologic function of MHC molecules is to display peptide fragments of proteins for recognition by antigen specific T cells.

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7
Q

MHC gene location

A

In humans the MHC complex genes are found on chromosome 6 and are also known as the human leukocyte antigen (HLA) complex as they were initially detected on leukocytes.

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8
Q

Where are MHC gene products found?

A

All mature cells except RBCs

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9
Q

Class I MHC molecules

A

Coded by HLA-A, HLA-B, and HLA-C genes; display antigens that are recognized by CD8+ T-lymphocytes and NK cells

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10
Q

Class II MHC molecules

A

Coded by HLA-DP, HLA-DQ, and HLA-DR genes; display antigens that are recognized by CD4+ T lymphocytes

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11
Q

Uses of HLA testing

A
  • Can be used to determine disease risk

- Used in transplantation work-up

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12
Q

Light chain restriction

A

Kappa or Lamda typein B cells. Ig light chian expressed by neoplastic, monoclonal B cell population.

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13
Q

Ways to detect light chain restriction

A
  • Flow cytometry
  • Serum protein electrophoresis with immunofixation electrophoresis
  • Kappa and lamda in situ hybridization study
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14
Q

Flow cytometry

A

-performed on fresh and unfixed tissue, blood, or body fluids.

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15
Q

Can exogenous or endogenous self-antigens elicit a hypersensitivity reaction?

A

Both

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16
Q

What usually causes a hypersensitivity reaction

A

Imbalance between the effector mechanisms of immune responses and the control mechanisms that serve to normally limit such responses. Often associated w/inheritance of particular susceptibility genes (HLA an non-HLA genes)

17
Q

What is the problem with hypersensitivity?

A

The reactions are poorly controlled, excessive, or misdirected.

18
Q

Immediate (Type 1) hypersensitivity reaction

A
  • IgE mediated activation of mast cells with degranulation and release of mast cell contents.
  • first step: sensitization
  • repeat exposure causes mast cell degranulation
  • Late phase reaction occurs when activated eosinophils secrete major basic protein and eosinophil cationic protein (toxic to epithelial cells) and activate mast cells to release mediators
19
Q

Antibody-mediated (type II) hypersensitivity

A

-Caused by Ab that react with normal or altered cell surface antigens in the extracellular matrix

20
Q

Atopy

A

Predisposition to develop immediate hypersensitivity reactions

21
Q

Hygiene hypothesis

A

Postulation that improved hygiene has diminished exposure to microbial antigens in early life that “educate” the immune system, setting stage for pathologic allergic responses later in life.

22
Q

Goodpasture syndrome

A

Circulating autoantibodies to antigens intrinsic to the glomerular basement membrane results in antibody mediated injury. Resulting anti-GBM immune complexes can be visualized with immunoflourescence microscopy as a linear pattern of deposition.

23
Q

Pemphigus vulgaris

A

Due to antibodies directed against desmogleins 1 and 3 (found in the desmosome)

24
Q

Immune complex mediated hypersensitivity (type 3) Steps

A

Immune complex formation
Immune complex deposition
Immune complex-mediated inflammation and tissue injury

25
Q

T cell mediated (Type IV) hypersensitivity

A

Caused by inflammation resulting from cytokines produced by CD4_ T lymphocytes and cell killing by CD8+ lymphocytes. Sensitized to exogenous or endogenous antigens

26
Q

2 mechanisms of type IV hypersensitivity

A

CD4+ T cell mediated inflammation. CD8+ T cell mediated immunity.

27
Q

CD4+ T cell-mediated inflammation

A

Response to repeat exposure of antigen, CD4+ cells secrete cytoines and cause recruitment and activation of macrophages and neutrophils causing an inflammatory response that can cause tissue injury

28
Q

Example of CD4+ T cell-mediated inflammation

A

Delayed-type hypersensitivity reaction. (Tissue reaction to antigens given to immune individuals)

29
Q

CD8+ T cell mediated immunity

A

CD8+ cytotoxic T cells kill antigen expressing target cells

30
Q

Granulomatous Inflammaiton

A

Distinctive patern of chronic inflammation. Usually results from a strong activation of T lymphocytes, leading to activated macrophages and causing tissue injury

31
Q

Granuloma

A

Focus of chronic inflammation consisting of microscopic aggregation of macrophages transformed into epithelial-like cells (histiocytes).

32
Q

What can histiocytes fuse to form?

A

Multi-nucleated giant cells

33
Q

What are granuloms the result of?

A

Immune reaction or a reaction to a foreign material

34
Q

Foreign body granulomas

A

See foreign material within histiocytes/giant cells.

35
Q

Caseating granulomas

A

Induce cell-mediated immune response w/central necrosis. Usually associated with infection