Term
Three classes of effector T cells to deal with multiple types of pathogens. |
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Definition
CD8:Kill infected cells displaying foreign Ag, typically virus infected cells.
CD4 (TH1): Stimulate macrophages
to kill intracellular pathogens.
CD4 (TH2): Stimulate
antibody production to facilitate elimination of extracellular pathogens.
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Term
Th1 cells can activate macrophages at the site of infection. |
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Definition
Effects of Macrophages:
MHC Class II Increases
TNF Receptors Increase
Oxygen Radicals Increase
Nitric Oxide Increases
These changes activate the macrophages to become highly microbicidal. Important because so many pathogens can replicate in macrophage vessicles. |
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Term
natural killer (NK) cells |
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Definition
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Activated by interferons – thought to act primarily during the early stage of infection, but can influence adaptive responses.
Inhibited by MHC Molecules
Stimulation of NK cells is not antigen specific – it is mediated by an ‘activation receptor’.
Interaction with any MHC molecule (not specific) inhibits the cytotoxic activity of NK cells.
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Term
Two Reasons why NKT are Inhibited by MHC |
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Definition
Two reasons :
a. prevents killing of host
cells, because they
typically express MHC
b. enables killing of cells
that don’t express MHC
-some viruses downregulate MHC expression as a
means to avoid detection by T cells |
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Term
Primary T cell responses to most infections |
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Definition
Three phases :
1. activation and expansion – 100 to 50,000-fold expansion
2. death (“AICD”) – 95% of cells die
3. memory (stability) – cells maintained at low frequency |
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Term
Secondary T cell responses to most infections |
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Definition
Compared to primary responses, memory responses are :
1. Higher frequency of antigen-specific cells (~1000x)
2. Faster (due to changes in gene expression)
3. Develop effector cells more efficiently (ie, requires lower Ag doses) |
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