AND ANSWERS
How to distinguish between NK and T cells? - ANS NK cells rely on diverse repertoire of
surface receptors to decide fate of target, whereas T cells rely on one unique TCR
- CD56 is also found on NK and T cells
-- presence of CD56 without TCR indicates NK cell
How are NK cells activated? - ANS needs 2 different activating receptors to be triggered
- binding IgG through CD16 is a high confidence message
Killer-cell Immunoglobulin-like Receptors (KIR) - ANS NK cell receptors that detect HLA-A/B/C
allotypes
- activates or inhibits NK cell response
KIR detects one of 4 shapes of HLA
γ:δ T cells - ANS goal is to be flexible and bind to variations of certain "themes" -- tissue
maintenance
- themes: certain types of molecules acting as signals
γ:δ T cells have fewer V(D)J blocks therefore less binding variability
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, γ:δ T cells % of blood lymphocytes - ANS humans: 5%
What are superantigens and how do they disable to immune system? - ANS highly toxic
proteins secreted by bacteria to intentionally stimulate T cell activation
- causes non-specific TCR-to-MHC binding of CD4 T cells --> overloads system
How do bacterial proteins such as SSLP7 interfere with IgA function? - ANS staphylococcal
superantigen-like protein 7 binds IgA and C5
- prevents phagocytosis and blocks C5-mediated MAC formation
Epstein Barr Virus (EBV) - ANS herpes virus that causes mononucleiosis
- after primary infection is beaten, EBV enters latency and is present for life
Severe Combined Immunodeficiency (SCID) - ANS lack T cell-dependent antibody responses
and T cell effector responses
Understand importance of CD4 and CCR5 as receptors that bind HIV. - ANS HIV bind to CD4
receptors and CCR5 co-receptors on host cells
Highly Active Anti-retroviral Therapy (HAART) - ANS combination therapy for HIV infection, in
which several antiviral drugs are used together to try and avoid the rapid generation of drug-
resistant mutant viruses that occurs when one of the drugs is used alone.
CCR5-Δ32 - ANS CCR5-Δ32 individuals are immune to HIV
- thought to give protection against bubonic plague and small pox
Type I Allergies: IgE and Mast cells - ANS - antigens bind to IgE on mast cells
- receptors MUST cross-link to send signal into cytoplasm
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- cell degranulates and releases mix of inflammatory molecules
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, considered immediate hypersensitivity because reaction is very fast and can be life-threatening
Type II Allergies: B cells and Macrophages - ANS - chemicals introduced to the body result in
altered presentation of cell antigens
- naive B cells recognize antigen as "non-self" and initiate IgG production
- macrophages attack self cells, resulting in tissue damage
Type III Allergies: B cells and Neutrophils - ANS - antibodies cross-react and form complexes
in blood
- may attach to tissues and result in improper fixation of complement and targeting by effector
cells
*usually occurs with immunotherapy when large amounts of Ig are introduced
Type IV Allergies: Dendritic cells and T cells - ANS - external molecules form adducts with
normal proteins, altering their form
- altered proteins are presented to CD4 T cells and activate phagocytosis and CD8 T cell attack
Mast cells - ANS detect infection, stimulate inflammation, repair damage
- located in tissue, not blodd
- contains granules with proteases and cytokines
mucosal mast cell: releases tryptase against microbes
connective tissue mast cells: releases chymotryptase to remodel tissue
Eosinophils - ANS has highly toxic pre-formed compounds to attack microbes
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- highly damaging to surrounding tissues
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