Term
| Mucosal infections are responsible for how many deaths of children under five annually? |
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Definition
| 10 million (4 million preventable by vaccine) |
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Term
| Why are mucosal tissues more vulnerable than skin? |
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Definition
| pathogens can survive longer in moist environments |
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Term
| T/F Hormones can influence the immune response of the female genital tract. |
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Definition
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Term
| What are immune inductive sites? |
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Definition
| nearby follicles or draining lymph nodes |
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Term
| T/F There are cells specialized for uptake of luminal antigens in all mucosal surfaces. |
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Definition
| True (M cells in intestines and dendritic cells in all) |
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Term
| How does simple columnar epithlium protect against pathogens? how is it vulnerable? |
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Definition
| they have a single impermeable layer of cells with tight junctions. However, it can easily be traumatized allowing pathogens to directly enter the host |
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Term
| How do non-keratinised stratified squamous epithelium protect against pathogens? What are the disadvatages to this strategy? |
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Definition
| mutliple layers reduce vulnerability. However they don't have tight junctions and are more permeable to small pathogens like viruses |
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Term
| Name the two goals of the mucosal immune system. |
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Definition
| Sterile protection and local containment |
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Term
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Definition
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Term
| Whats the difference between outer and inner mucus layers? |
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Definition
outer is loosely adherent with degraded mucus and most commensals are here
inner is firmly adherent to mucosal surface and has concentrated IgA and antimicrobials and some commensals |
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Term
| How do natural flora protect us? |
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Definition
| 1)compete for attachment sites on epithelial cells 2)competition for nutrients 3) production of growth inhibitors |
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Term
| How does lactobaccilli inhibit growth via production of growth inhibitors in the female reproductive tract? |
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Definition
| lactobaccilli makes lactic acid to lower the pH |
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Term
| List the cells that act as general innate effectors of the mucosal immune system. |
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Definition
| NK cells, macrophages, neutrophils, monocytes, dendritic cells |
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Term
| T/F Epithelial cells are not responsible for producing cytokines. |
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Definition
| FALSE. epithelial cells produce cytokines including chemokines in the mucosal surfaces |
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Term
| The lamina propria is populated by what kind of T cells? |
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Definition
| resting memory cells or recently activated T cells |
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Term
| How do epithelial cells screen for PAMPS? What do they do once they sense them? |
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Definition
| via basolateral TLR and intracellular nucleotide-binding oligomerization domain (NOD) proteins. They then secrete chemokines to attract neutrophils and monocytes from blood |
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Term
| In what tissues can you find M cells? Where in those tissues? |
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Definition
| in the tonsils and intestines, near the dome region of local follicles |
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Term
| T/F The apical surfaces of M cells are covered with mucus. |
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Definition
| FALSE, the apical/luminal surfaces are exposed |
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Term
| How do m cells bind antigens? |
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Definition
|
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Term
| Besides M cells, what other cell captures luminal antigens? |
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Definition
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Term
| T/F In the intestines, immune inductive sites are adjascent to immune effector sites. |
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Definition
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Term
| How do lymphocytes know to go to the mucosal surface associated with the infection? |
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Definition
| DC imprint tissue-specific "signature" on activated naive lymphocytes, which up-regulates homing receptors. After going through circulation, they bind to HEV expressing both their homing receptor adhesion molecules and tissue-specific chemokines. They also migrate towards epithelium where concentrations of tissue-specific chemokine are greatest |
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Term
| Where do activated B and T cells go once they leave the mucosa? |
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Definition
| Peyer's patch or local lymph aggregation>efferent lymphatics>lymph node>circulation>HEV>tissue |
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Term
| What chemokines/receptors are given to activated lymphocytes to help them find the small intestine? |
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Definition
lymphocytes express alpha4beta7 and CCR9 chemokine receptor.
This binds to MADCAM on HEV and the CCL25 chemokine |
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Term
| Why is mucosa rich in IgA? |
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Definition
| TGF-beta is a molecule that helps suppress the immune system at mucosal surfaces and incidently causes local mucosal plasma cells to switch to making IgA |
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Term
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Definition
| Secretory-IgA, consisting of IgA dimer with a secretory component added by the epithelial cells that have transported IgA to their apical surface |
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Term
| Why is mucosal IgA dimeric or tetrameric? |
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Definition
| in order to bind the poly-Ig receptor on the epithelial cell, IgA needs a J chain. J chains are only found on polymeric IgA |
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Term
| How does secretory IgA help prevent infection? |
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Definition
| can bind and neutralize pathogens and toxins either in the lumen or internalized in endosomes of epithelial cells. ALso, IgA can export toxins and pathogens from the lamina propria WHILE being secreted, neutralizing viruses or toxins in the lamina propria |
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Term
| Besides IgA, what other Ig helps neutralize pathogens in the lamina propria? |
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Definition
| serum IgG can transudate into the lamina propria via fenestrated capillaries |
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Term
| What is the incidence of people with IgA deficiency? |
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Definition
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Term
| How do people with IgA deficiency compensate? |
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Definition
| they make more defensins and transportable IgM (patients lacking pIgR are worse off because secretory antibodies are very important!) |
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Term
| What types of cells characterize inductive sites? effector sites? |
|
Definition
inductor=naive cells
effector=plasma cells and activated T cells |
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Term
| Which cells/Igs help downregulate inflammatory response in mucosal surfaces? |
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Definition
| phagocytic but noninflammatory macrophages, tolerance inducing DC and T cells, and noninflammatory IgA antibody |
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