Term
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Definition
o Immune system attacks own tissue. An individual’s immune system recognizes its own cells as foreign and mounts an immune response that injures self tissues. |
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Term
| 4 theories of autoimmunity |
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Definition
- Antigenic mimicry theory
- Release of sequestered antigens
- T-cell theories
- B-cell theories
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Term
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Definition
§ Self/foreign antigens made of same materials, so alterations in self tissue lead to attack |
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Term
| Release of sequestered antigens |
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Definition
§ Self antigens not in direct contact with lymphocytes during fetal development
§ Antigens “hid” in places lymphatics couldn’t reach, when illness hits, Ag’s released |
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Term
| T-cell theories (autoimmunity) |
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Definition
§ Thymus gland defects
§ Decreased suppressor T-cell function
§ Altered T helper cell function |
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Term
| B-cell theories (autoimmunity) |
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Definition
§ B cells lose their responsiveness to suppressor T-cell signals: ↑↑ in B cell function and autoAb production |
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Term
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Definition
Ø : Normal immune response that is:
o Inappropriately triggered
o Excessive
Produces undesirable effects on the body |
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Term
| Basic mechanism of hypersensitivity |
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Definition
o specific antigen-antibody reaction or specific antigen-lymphocyte interaction |
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Term
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Definition
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Term
| Type 1 hypersensitivity: primary Ab and role of intracellular Ca++ |
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Definition
IgE
Increases intracellular Ca++ |
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Term
| Type 1 hypersensitivity: how long does it take? |
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Definition
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Term
| Type 1 hypersensitivity: Principle WBC, principle chemical mediator |
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Definition
§ Mast Cell
§ Histamine: causes increased vascular permeability, vasodilation, urticaria, smooth muscle constriction (asthma!), increased mucus secretion, pruritus |
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Term
| Type 1 hypersensitivity: Steps of reaction (7) |
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Definition
§ Ag (antigen) exposed to B cells
§ B cells crank out IgE
§ Ige binds to mast cells (covered with IgE receptors/vesicles filled with vasoactive substances)
§ Exposure of mast cell to Ag→IgE and Ag’s crosslink
§ ↑ intracellular Ca+2
§ Degranulation
§ Inflammation |
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Term
| Type 1 hypersensitivity: clinical manifestations (mild, moderate, anaphylaxis) |
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Definition
§ Mild
· Hives
· Seasonal allergic rhinitis
· Eczema
§ Moderate
· Throat constriction
· Wheezing
· Tachycardia
§ Anaphylaxis
· Most life-threatening reaction; occurs in very small number of highly allergic individuals
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Term
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Definition
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Term
| Type 2 Hypersensitivity: primary Ab's involved |
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Definition
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Term
| Type 2 Hypersensitivity: How is tissue damage accomplished? |
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Definition
§ Antibodies attack antigens on surface of specific cells or tissues |
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Term
| Type 2 Hypersensitivity: antigens and Ab's associated with blood types |
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Definition
§ Type A
· A Ag and B Ab
§ Type B
· B Ag and A Ab
§ Type AB
· A/B Ag and no Ab
§ Type O
· No Ag and A/B Ab |
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Term
| Type 2 Hypersensitivity: Erythroblastosis fetalis (mechanism) |
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Definition
§ Rh-neg mother is pregnant with Rh+ baby → blood mixes at delivery → mom makes antiRh-Ab → (next pregnancy) Rh-neg mother pregnant with Rh+ baby → mother’s IgG crosses placenta and attacks fetal blood cells |
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Term
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Definition
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Term
| Type 3 Hypersensitivity: primary Ab involved |
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Definition
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Term
| Type 3 Hypersensitivity: How does tissue damage occur? |
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Definition
§ Immune system is unable to get rid of Ab-Ag complexes, complexes deposit in tissue and complement/neutrophils are activated which results in the release of enzymes and free radicals resulting in tissue destruction |
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Term
| Type 3 Hypersensitivity: Where do complexes collect |
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Definition
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Term
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Definition
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Term
| Type 4 Hypersensitivity: Principal mediators |
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Definition
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Term
| Type 4 Hypersensitivity: what is hapten? |
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Definition
| Incomplete, lipid soluble antigen |
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Term
| Type 4 Hypersensitivity: describe the mechanism (6) |
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Definition
§ Hapten binds with another ‘carrier’ protein (hapten+protein=complete Ag)
§ Ag taken up by Ag-presenting cell
§ Taken to lymph node
§ Presented to Th cells
§ Lymphokines released
§ Inflammation→destruction |
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Term
| Type 4 Hypersensitivity: which branch of immune response? |
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Definition
| Adaptive, so it takes time |
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Term
| Type 4 Hypersensitivity: how is tuberculosis a type 4 hypersensitivity reaction? what happens? |
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Definition
§ The Ag is not destroyed by macrophage→triggers inflammatory response→ immune cells begin to collect and build up forming a giant multi-nucleated cell (granuloma)→ granuloma becomes fibrotic→ central necrosis (caseous) |
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Term
| Chronic mucocutaneaus candiasis |
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Definition
o Autosomal recessive; a selective deficiency of cell-mediated immunity against C. albicans |
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Term
| Primary immunodeficiency disorder |
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Definition
§ May be from congenital, genetic, or acquired defects that directly affect immune cell function
§ First clinical indicators: signs and symptoms of infection
§ Suspected with severe recurrent, unusual, or unmanageable infections
§ Most cause moderate immune impairment that may not be diagnosed
§ Severe congenital immunodeficiency disorders less common, clinically significant |
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Term
| Secondary immunodefiency disorder |
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Definition
§ Problems in neuroendocrine and immune system interaction
§ Excessive neuroendocrine response to stress; increased corticosteroid production increases susceptibility to infection
§ Immune function impaired as a result of other non-immune system disorders that secondarily suppress immune function
· Poor nutrition
· Stress
· Drugs |
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Term
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Definition
o Self-tolerance=recognition; so autoimmunity= break down of self-tolerance |
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Definition
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