Term
| How do CD4+ Helper T cells work? |
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Definition
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Term
| how do CD8+ cytotoxic T cells work? |
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Definition
| killing cells containing microbes. |
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Term
| when a microbe resists phagocytotic killing and lives in vesicles or cytoplasm, what can they be referred to as? |
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Definition
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Term
| where do you find adhesion molecules and chemokine receptors? |
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Definition
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Term
| where do you find adhesion molecule ligands and the production of chemokines? |
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Definition
| Endothelium. (increased expression after exposure to microbes). |
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Term
| where are high endothelial venules found? |
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Definition
| lymphoid organs. allow for passage of T cells into node. |
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Term
| how do we get T cells out of lymph node? |
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Definition
| decreasing their level of chemokine receptor expression. (same process as to how they leave the HEV and into a lymph node) |
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Term
| what are the different classes of molecules involved in T cell migration into/out of Lymph nodes? |
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Definition
| Chemokines, chemokine receptors, Adhesion molecules, adhesion molecule ligands. NONE of these are antigen specific. |
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Term
| why allow so many T cells into lymph node? |
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Definition
| maximize ability of T cells to search out microbe since frequency of effector is still relatively low. |
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Term
| when T cells run into an incorrect antigen, do you see an increase in adhesion molecule expression? |
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Definition
| No. The cells simply return to circulation to look for their correct antigen. |
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Term
| Do differentiated effector cells need co-stimulation? |
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Definition
| No! Infected cells don't express co-stimulatory molecules (likeB7). That job is for APCs. |
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Term
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Definition
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Term
| How do CD4+ Th1 cells activate macrophages? |
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Definition
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