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week 7 notes 390

by: Mary-elizabeth Notetaker

week 7 notes 390 bio 390

Mary-elizabeth Notetaker
U of L

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About this Document

week 7
Intro to Immunology.
Shira Rabin
Class Notes
Bio, Biology, bio390, introtoimmunology, immunology
25 ?




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This 2 page Class Notes was uploaded by Mary-elizabeth Notetaker on Thursday October 6, 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 8 views. For similar materials see Intro to Immunology. in Biology at University of Louisville.


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Date Created: 10/06/16
Week 7 Thursday, October 6, 20161:01 PM • MHC- used for antigen presentation by all cells except RBC (named bc of transplanted tissue-self marker) ○ Antigen + MHC for T cell recog  TCR needs diff cell w MHC and the antigen in the MHC(MHC holding antigen) in order to bind ○ Classes:  Class I- cytosolic proteins (most nucleated cells)… ME proteins on ME molecule □ … lung/skin/general cells will have MHC class I on them Will randomly take up things in cell to be presented… allows body to see what is in the cell Ex) like a virus, etc… if virus will have virus antigen present to show infection) □ Intracellular things(usually self proteins) □ Stx:  A chain ◊ 3 external domains(a1,a2,a3) ◊ Cytoplasmic domain ◊ A1,a2 domains form cleft to bind peptide antigen  B2- microglobulin ◊ No trans-memb domain ◊ Non-covalently bound to a chain  On outside of cell ◊ Critical to fx, even tho doesn’t bind to peptide  Exon/intron arrangement ◊ 5' leader exon for signal peptide followed by 5/6 exons  Leader region(sends to ER)--Signal peptide is removed in ER (then to cell plasma memb) ◊ Immunoglobulin fam (circular regions)= antibody  Peptide bound enclosed, doesn’t stick out  Class II- APCs… external proteins that have been phagocytosed □ Phagocytes… bring in microbe & destroy it. Bits of microbe will be on its cell surface □ Extracellular things □ Stx:  A & b chains  Both chains pass thru plasma memb ◊ External ◊ Trans memb ◊ Cytoplasmic  A1 & b1 domains form peptide binding cleft  Both a & b genes have leader exon  Peptide bound bigger, not fully enclosed ○ Polymorphism of MHC  Several hundred diff allelic variants □ 6 class I mols □ 12 class II molsexpressed per person □ NOT the specificity characterized by Ag-Ab & Ag-TCR  Promiscuity- MHC mol can bind many diff peptides(antigens), and some peptides(antigens) can bind to many diff MHC mols □ If cant bind peptides, cant present to t cell, so t cell not activates = issues • MHC interactions w peptides ○ Class I ( to remember, class 1 x CD8= 8)  Present peptides to CD8+ t cells □ Kill cells.. Majority will not get response bc have MHC… insurance policy--> always checks anyways  Peptides derived from endogenous intracellular proteins (mostly self)  Some AA anchor the peptide, others interact w TCR  Smaller peps that fit entirely inside 2 alpha helices w one small area in btwn somewhat exposed (heads touching and both ppl under covers)  Anchor residues- buried inside pep groove… ("tucked under the covers"…feet) □ Typical pep: 8-9 AAs □ 2nd & last AA residues imp for binding MHC I(often hydrophobic) □ Class I binds peps of diff lengths-->diff bulges… bulge intxs w TCR ..pep held in closed config ○ Class II( to remember, class 2 x CD4=8)  Usually derived from exogenous ex cellular processed antigens.. Can be self peps  Present antigen peps to CD4+ T cells □ AA residues to intx w TCR  13-18 AAs.. Will stick out end-->"open conformation" Bio 390 Page 1  Usually derived from exogenous ex cellular processed antigens.. Can be self peps  Present antigen peps to CD4+ T cells □ AA residues to intx w TCR  13-18 AAs.. Will stick out end-->"open conformation"  No conserved anchor residues, bc not anchored □ So have H bonds distrib'd thru middle 7AAs..bind certain residues here to hold it in groove  Elevated off "floor" in open config.. Held up on top of binding pocket  Flexibility contributes to promiscuity • Binding to peps ○ BCR & TCR- genomic arrangement  Couple hundred genes, few selected to form BCR/TCR… lots of variation …after selection, that’s it: it is the binding pocket ○ MHC mols- binding promiscuity  Expression of diff MHC mols on every cell  Max chances that many diff epitomes will be recognized • 3 classes of mols- MHC in every vertebrate species  HLA in humans- what was picked for each slot in this person □ Helpful in matching transplant organs  H2 complex in mice ○ Class I: on all nucleated cells, present endogenous antigens to CD8+ T cells ○ Class II: on APCs, present exogenous antigens to cd4+ ○ Class III: components in complement & inflamm (C4, C2, factor B) • Haplotype inheritance- 1 from each parent ○ Haplotype- allelic forms of MHC genes inherited in linked groups ○ If mice inbred, standardizes MHC genotypes- syngenic (same)  9 from each parent, 18 total  Ex) bb x kk inbred mice --> all offspring bk Problem: bk couldn’t give organ to either parent bc has half diff haplotype  Genetically linked, inherited together.. Only 25% chance offspring are same haplotype to each other □ From ab x cd--> many diff phenotypes • Co-dominant expression- MHC alleles co-dom expressed ○ Both maternal and paternal MHC genes are expressed in offspring cells..  Good: Want everything on table to all can be used..present as many antigen peptides as possible  Bad: makes transplantation diff bc humans hetero at each locus • MHC diversity in indivs ○ Polymorphism has fx relevance ○ Diff tend to be clustered at AA locations w/in groove sites Bc if areas in grooves were changed too much, confo may not bind anything  Bio 390 Page 2


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