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This 4 page Class Notes was uploaded by Hojoong Notetaker on Tuesday January 5, 2016. The Class Notes belongs to Drama 103 at University of Washington taught by Jason Eckard in Fall 2016. Since its upload, it has received 51 views. For similar materials see Theatre Appreciation in Theatre at University of Washington.
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Date Created: 01/05/16
Week 8 Quiz Section Mucosal surfaces are the primary sites of pathogen invasion Most pathogens invade through mucosal surfaces (mouth, airways, digestive systems) Collectively, mucosal tissues = MALT Specialized areas = BALT, GALT, Organization of mucosal immune cells in gut You have villi and there’s only a single cell layer that separates gut lumen from the tissue below Specialized M cells are present in this epithelial layer Mucosa characterized by active antigen uptake/sampling M cells can bring in antigen by endocytosis, phagocytosis, and transcytosis Once brought in, bound by dendritic cells which can present and activate to T cells M cells have folds on the basolateral side where lymphocytes can hang out and be ready to respond Nonspecific transport by M cells There are 4 main ways to bring in antigen: Fcdependent transport: antibodies bind antigen in the lumen, then internalize the antigen to present to DC Apoptosisdependent transfer: if a cell is infected, it can become apoptotic and release antigen as a part of this process Antigen capture: immune cells (particularly DC) can extend past the layer and sample the gut lumen T cell activation in the MALT 1. DC picks up antigen, presents to naïve T cell 2. Naïve T cell will extravasate out of peyer’s patch in to blood 3. Once T cell finds antigens, will change expression of receptors; this means once they express these new receptors, they aren’t honed to HEV, but rather to mucosal area of gut epithelial cells T cells activated in the mucosa return via the blood MAdCAM1 on endothelium cells mediate transport of T cell from blood vessel into the lamina propria T cells then express different receptors to determine if it’ll go into large intestine or large intestine CCR9 small intestine (CCL25) CCR10 large intestine (CCL28) Ecadherin on both large and small Mucosal immune cells reside in distinct compartments Two types of IELs Type A: Traditional CD8: bind MHC class I + cognate antigen lyse of epithelial cell Type B: Cd8a:a, restricted TCR: instead of using TCR to determine pathogen killing, have a different array of receptors that are often seen on NK cells. Still lyse via perforin/granzyme, but use NKG2D and bind MICA:B instead Mucosal IgA neutralizes antigens IgA is unique to mucosal surfaces Dimer connected by J chain B cells activated in mucosa will go through class switch primarily to IgA Example of mucosal immune response (diagrams) Grey = lymphatics, red = blood 1. Salmonella in gut from eating bad food. Antigens from salmonella are shed and transported through M cell to Peyer’s patch through one of the 4 mechanisms we discussed 2. In PP, these antigens are processed by DC which then present Ag/peptide fragments via MHC 3. Naïve T cells enter PP at the HEV through blood using CCR7/LSelectin a. If this T cell is specific for the antigen presented by the DC, the TCR will bind to the antigenMHC complex which will induce changes in the receptors expressed by the T cell (CCR9/10, LFA1, etc), 4. T cell exits PP through lymphatics, then goes to thoracic duct and is dumped back into blood circulation 5. Once in blood circulation, activated T cells will hone to the gut since it’s expressing AE B7, where it will initiate an immune response a. If it interacts with E cadherin, stabilizing the T cell 6. You can also have immune sensors like TLR4 and 5 and cytosolic receptors like NOD1/2; these all can result in inflammatory response that secretes IFNa 7. If the epithelial cells are infected and detected through TLR sensing Infected enterocyte & CD8 T cell Present MHC I by infected enterocyte and detected by CD8 T cell Induces cell killing by FasFasL complex as well as Perforin/Granzyme/Granulysin mechanism Mechanisms of Immune Evasion HCV as a model of pathogen evasion of the innate immune response HCV PAMPs are sensed by the innate immune system Heaptocytes: main stromal liver cells Kupffer cell: specialized macrophage only found in liver HCV enters and is detected by TLR3 or RIGI sensors, resulting in IFN / immune response HCV can also be taken up in exosomes in DC which activate TLR7 and results in pro inflammatory cytokines Phagocytosis of HCV can result in TLR7 activation and NLRP3 activation (by detection of damage to cell) inflammatory state IL1B which is great at destroying cells which is what wreaks havoc in HCV patients Global prevalence of chronic HCV infection remains high There is an extremely effective antiviral but it’s too expensive for mass use as of now microRNAs can bind to regulatory (noncoding) elements in mRNA transcripts and inhibit their translation miRNA has an inhibitory role and can bind mRNA to create a dsmRNA that is nonfunctional Directly blocks translation of that protein Normally produced by host Type III IFN are secreted in response to viral infection, but their effect is primarily targeted to the liver and mucosal epithelial cells Specific to liver as most receptors for TypeIII IFN are present only in liver This is an IFN induced specifically during HCV infection HCV can inhibit antiviral response by inducing production of hostderived miRNAs that prevent IFNL3 translation With no IFNlambda, the immune response is deficient and HCV persists miRNA binding to mRNA is dependent on a single nucleotide (T/G) Main Takeway for Host/Pathogen infections Constant battle between detection/elimination and evasion/antagonism Allergy and Hypersensitivity Allergy: an inappropriate immune response to an antigen that doesn’t actually cause harm to your body Type I allergic response mediated by Mast Cells and IgE Induced by activation of B cells to specifically produce IgE Ab once plasma cells secrete IgE, IgE will coat mast cells through Fcepsilon receptors Fab part of the receptor is ready to bind antigen; mast cells are primed Once binds, strong, rapid response by mast cell to secrete toxic granules Type II allergic response mediated by destruction of IgGbound cells, either through complement or CTLs 2 results: Surface antigen from allergen expressed on cell; an antibody bound to the surface antigen will also bind the Fc receptor on the CTL, which will then lyse the cell If the surface antigen (still bound by IgG) can activate complement Type III mediated by IgG Ab/Ag complexes Formation of immune complex (soluble antigen in solution + antibodies = aggregation = formation of immune complex highly immunogenic, activating complement which will recruit inflammatory neutrophils) Type IV Mediated by T cells (different from Type II), demonstrating direct T cell response NOT a soluble antigen that is presented to T cells, but presented through MHC (picture is misleading) T cell which is specific to something like pollen is sensitized and binds it’s antigen, dumps cytokines which activate other cells in the surrounding area. For this to occur, need a T cell response which takes a lot more time. Result: cellmediated hypersensitivity and tissue destruction mediated by these effector cells that are initiated by CD4 T cells Type II: penicillin allergy Penicillin will coat the surface of RBCs, creating a new antigen that appears to the body as foreign, activating your immune response, enhancing complement fixation and coating of bacteria as well as by RBC PenicillinRBC taken up by macrophages, phagocytized, and presented to T cells T cells that recognize these penicillinRBC will lyse the RBC Type IV: Celiac Disease 1. Normally, you have gluten that is digested by enzymes in the gut lumen, producing a gluten fragment 2. Gluten is normally not detected by immune system, and shouldn’t be presented by MHC. In Celiac’s, gluten IS presented by MHC and causes a T cell response to gluten a. This can happen because you have expression of specific HLA genes (e.g. HLA DQ) that are more able to present gluten peptides b. Also, you have TTG that is a normal enzyme expressed by intestines. For Celiac’s, this enzyme has an inappropriate function (not sure if it’s because if we have too much TTG or if it’s acting weird) and causes deamination of gluten which allows it to be presented through MHC pathway c. Hallmark of Celiac: autoantibodies against TTG. Unknown if antibodies themselves are enhancing pathology or if they are a bydproduct of having too much TTG. It all comes down to MHC presentation of a peptide that you shouldn’t be presenting (gluten) since it’s modified by TTG 3. End result: cells presenting gluten and activates a T cell response specific to gluten which destroys epithelial cells a. HLADQ is expressed by 90% of Celiac’s
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