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week 8 390

by: Mary-elizabeth Notetaker

week 8 390 bio 390

Mary-elizabeth Notetaker
U of L

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week 8
Intro to Immunology.
Shira Rabin
Class Notes
Bio, bio409, immunology, introtoimmunology, UofL
25 ?




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This 3 page Class Notes was uploaded by Mary-elizabeth Notetaker on Sunday October 16, 2016. The Class Notes belongs to bio 390 at University of Louisville taught by Shira Rabin in Fall 2016. Since its upload, it has received 7 views. For similar materials see Intro to Immunology. in Biology at University of Louisville.


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Date Created: 10/16/16
Week 8 Tuesday, October 11, 2016 10:53 AM  DFTD- fatal cond in Tasmanian devils, die w in month from starvation ○ Transmittable- passed as allograft(tissue cell that is not self) during mating from biting ○ Distinct from all other cells..arose in singleanimal and spread rather than occurring in each animal  Tasmanian devil cell w tasmanian dna, but mhc marker is different from all others ○ Infected devils did not recognize lymphocytes from other devils as non-self ○ Cancer acts as microbe  Mhc diversity w in species: ○ 10^9 class 1 haplotypes possible ○ 10^15 class 2 combos ○ Total: 10^24 combos w in humans  MHC genetic features ○ Ensure diversity: polygeny(many genes), promiscuity, codominant expression(set from mom/dad… no recessive..both expressed) ○ Assoc btwn HLA allele & disease  High- ankylosing spondylitis,celiac disease (mhc binds too strongly)  AIDS(reverse)- mhc doesn’t bind virus well  Not as high- MS & RA (no assoc w mhc binding) ○ Cheetahs and panthers have low mhc diversity  Inbreeding, same mhc- infectious disease->everyone binds disease same way so immune resp same, if bad resp whole pop could be wiped out ○ Mhc and mouse urine odor- mhc mol smell-->can tell if diff/same mhc in mate ○ Women, contraceptives, and MHC- preferred men of same mhc, odd  Class 1 expression: low in liver(allows transplants to be more successful) ○ Intracellular proteins displayed: self, viral, altered-self cells  Class 2 expression: on APCs  T cell restriction: recog peptides in context of self-mhc ○ Mhc haplotype of presenting t cell mustmatch haplotype of t cell ○ So, imp for activating sis  Mhc expression patterns- #s change w changing conds ○ Infection ○ viral interference  NK cells-can tell there's issueif small # mhc on cell surface so kill it  Cancer ○ cytokine-mediated signaling(upor down)- play role in infection lvl  Costimulation-need extra support to activate t cell: ○ Mhc/Ag + tcr ○ CD80/86 +CD28 (costimulation markers)  When these cells present, mhc is activated more early  Mhc Class 2 expression patterns: ○ DCs most effective bc have high levels mhc & cd80/86 at all times ○ B cells: high mhc at all times, but only have CD80/86 after activation  Phago--> bind peptide->upreg cd80/86 .. Keeps b cell from being activated unnecessarily ○ Macs- need activation from TLR in order to express MHC & costim mols  Diff processing/presentation pathways ○ Class 1: endogenous processing (in RER)  Peptides generated by proteasomes (consitutive proteosome: B1, B2, B5) □ Ubiquitin- tags proteins to send to proteasome(trash disposal) □ Most proteins not presented □ Most proteins not presented  Immunoproteasome cleaves proteins into frags that pair better w mhc mols (B1i, B2i, B5i) □ In APCs and infected cells □ Upreg'd by cytokines (IFN, TNF) □ Exists fleetingly □ Inc'd protein degradation, so peptides find mhc to bind easier--> autoimmunity  Typical starting point: when peps transported from cytosol to rough ER □ TAP transporter- need atp, affinity for hydrophobic AAs □ Meet waiting mhc class 1 mol in rough ER  Chaperonins aid peptide/mhc class 1 assembly □ Calnexin, carleticulin, & taspain(assists in taking protein to TAP) □ ER aminopeptidase(ERAP) further processes peptides □ Alpha chain inserted into memb, taken to proteosome, hydrophobic tail shoots back in membrane, rest synth'd.. Class 1 mol, exits RER ○ Class 2: exogenous processing- phago'd protein coming in and meet w class 2 mol to get into pocket..needs to be brought to memb, but needs to go back to cell have mhc class 1 cells that should not be binidng mhc cells  Pep genp gen'd by internalized antigens  Invariant chain prevents endogenously derived peps from binding in RER  Lysozomal enzymes degrade proteins  When mhc class 2 mol done, will meet up w vesicle w peptides from antigen that was brought in and will degrade it □ Ii is degraded w/in endosome to CLIP □ HLA-DM exchanges CLIP for peptide □ HLA-DM exhanges peps, strongest assocs remain □ HLO-DO negative regulator, role in tolerance(diabetes study)  Be able to compare class 1 processing vs class 2 processing  Cross-presentation of antigens ○ Exogenous antigens are redirected to endogenous pathway ○ Allows presentation on mhc class 1 mols --> CD8+ t cell activation ○ DCs are only APCs w this ability: can take exo pep and put on both class 1 & class 2 mhc mols □ Class 2 mhc binds CD4 t cells □ Class 1 mhc bind CD8 t cells (produces IL2 cytokine)  Adv: can activate 2 cell types, helps immunesystem bc more things acting to get rid of microve  DC takes something in and CD4 tells to put it on mhc class 2 which produces IL2 cytokine which tells DC to put on class 1 □ Licensed DC cells can do this and maintains tolerance  Presentation of nonpep antigens ○ Some lipid Ag are recog by t cells  Presentation by CD1 fam of nonclassical class 1 mols □ 5 human cd1 genes □ Fx of mhc class 2 mols □ Fx of mhc class 2 mols


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