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28 Cards in this Set
- Front
- Back
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Where do the vast majority of pathogens invade?
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Via mucosal surfaces.
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What are inductive sites?
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Sites where T and B cells see (and get activated by) antigen. MALT. GALT is especially important - there are more bacteria in gut than all other combined.
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What are effector sites?
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Sites where cells induced in inductive sites actually go. Most of these are in lamina propria of mucosa. (e.g., nasal mucosa, upper respiratory tract, lacrimal glands, salivary glands, mammary glands, intestinal tract etc)
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What is the advantage of having tonsils?
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In the absence of tonsils poor immune response to polio vaccine is seen.
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What is Waldeyer's ring?
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A ring of lymphoid tissues (tonsils and adenoids) around the entrance to gut and airway
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What are lymphoid follicles primary aggregated in ileum?
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peyer's patches
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What are M cells?
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Specialized cells in the epithelium of Peyer's patches that appear flat/depressed. They function as facilitators of antigen entry. NOT antigen-presenting cells.
M cells hand off antigen to lymphocyte or dendritic cell. Enteric pathogens can exploit them. |
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What other way is there for antigen to be taken up in a mucosa?
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Sometimes dendritic cells extend processes between epithelial layer cells to capture antigen from gut lumen.
This is a secondary way for antigen to get taken up; primary way is thru M cells. |
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What is the primary way to capture antigen from gut lumen?
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M Cells. DCs are 2ndary way
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Lamina propria contains ______________(what type of immune cells) while epithelium contains __________.
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whole range of immune cells; CD8 T cells
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What are intraepithelial lymphocytes (IELs?)
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They make up 10-15% of epithelial cells; 90% of them are CD8 T cells; They have limited specificities.
Two types CD8 αβ and CD8 αα |
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What are the two types of intraepithelial lymphocytes (IELs?)
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CD8 αβ and CD8 αα
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Naive lymphocytes activated in peyer's patches give rise to effector cells that travel in the lymph and blood to gain access to _________________________
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lamina propria of the mucosal tissue.
Basically B and T cells that are activated in the inductive sites (PP etc) traffic to effector sites (intestinal lamina propria) via lymph --> blood ---> exit out blood via HEVs --> effector lamina propria |
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How is homing directed for the B and T cells in the gut?
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1) Gut homing effector T cells bind to intestinal vascular epithelium and enter lamina propria (Integrin (α4β7) : Addressin (MadCAM) )
2) In the lamina propria gut homing T cells bind to chemokines expressed by intestinal epithelium. ( Chemokine receptor CCR9: Chemokine (CCL25) interactions ) |
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Integrin (α4β7) interacts with what to do what?
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Addressin (MadCAM) to direct the T cell out of the venule
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When a cell is activated in a particular site (e.g., gut) what determines how the cell gets into the appropriate/same type of tissue?
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The particular integrin: CAM interaction
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How are mucosal epithelial cells an active barrier for bacteria/what happens when mucosal epithelial cells endocytose bacteria?
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1) Mucosal epithelial cells endocytose bacteria and interact with them in vesicles via TLR or NODS.
2) Activation of these receptors causes activation of NFκB 3) Promoters for a wide array of pro-inflammatory mediators (cytokines etc) are activated by NFκB 4) These mediators activate neutrophils, macrophages etc |
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What is the Hallmark of Effective Immunization Against
Enteric Pathogens? |
An IgA response
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What is the IgA response to enteric pathogens?
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It's pretty versatile and can do several things.
A) It can eliminate toxins from lamina propria while being secreted into gut lumen B) Blocks pathogens from attaching to epithelium in gut lumen (aka neutralization) when secreted C) Binds pathogen on M Cell surface to transport pathogen to lymphoid tissue (will lead to a better response being made) D) Can pick up antigen in endosomes and take it to lymphoid tissue |
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What are the different classes of IgA? How do they differ?
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IgA2 and IgA1. IgA2 is more resistant to proteases
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Which IgA is more resistant to proteases?
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IgA2
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What is the function of IEL CD8αβ cells?
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1) Virus infects mucosal epithelial cell
2) Infected cell displays viral peptide to CD8 IEL via MHC Class I 3) Activated IEL CD8 T cell kills infected epithelial cell via granzyme/perforin and Fas-dept. pathways. <b>They're similar to peripheral CD8 T cells in behavior.</b> |
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What is the function of IEL CD8αα cells?
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Function is to <b>kill stressed epithelial cells.</b>Very interesting cells.
Do not recognize antigen via MHC Class I. Do NOT undergo thymic selection; many are self-reactive. They're cytotoxic and express pro-inflammatory cytokines. |
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How do IEL CD8αα T cells kill stressed cells?
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1) Epithelial cells undergo stress as a result of infection, damage, etc. and <b>express MIC-A and MIC-B</b>.
2) NKG2D on innate immunity/sentinel cells bind MIC-A and MIC-B 3) Activated IEL kills the stressed cell. |
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What are functions of MIC-A and MIC-B?
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They're cytokines that are expressed by stressed cells (stress from infection, damage, etc.)
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How does the gut recognize commensal/good species from pathogenic species?
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Commensal species stimulate epithelium to produce cytokines that <b>inhibit dendritic cell maturation </b>. Immature dendritic cells induce T regulatory cells that express TGFβ.
Invasive bacteria stimulate dendritic cells to mature. Mature DCs produce T helpers. |
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What does the inhibition of dendritic cell maturation mean?
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It means the immature DC will stimulate t cells to become T regulatory cells --> no attack of pathogens (because they're good species)
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What produces TGFβ? What's its role?
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Produced by T regulatory cells. TGF-β appears to block the activation of lymphocytes and monocyte derived phagocytes.
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