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test 1 review 390

by: Mary-elizabeth Notetaker

test 1 review 390 bio 329

Mary-elizabeth Notetaker
U of L

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test 1 review
Intro to Immunology
Shira Rabin
Study Guide
Bio, bio390, immunology, introtoimmunology
50 ?




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This 9 page Study Guide was uploaded by Mary-elizabeth Notetaker on Monday September 12, 2016. The Study Guide belongs to bio 329 at University of Louisville taught by Shira Rabin in Fall 2016. Since its upload, it has received 46 views. For similar materials see Intro to Immunology in Biology at University of Louisville.


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Date Created: 09/12/16
 Vaccinations-induce immunity  Smallpox & cows  more active phagocytic cells in immunized animals(cellular component) ◦ non cell components were critical (serum)  Transferred resistance to diphtheria ◦Kabat- antibody transfers resistance ◦...immune system has cellular, noncellular, organ, and outside components..all the above combined  immune system ◦Innate immunity-immediate attack  Not specific ,ame response to repeat infection  Major component: barriers(skin)  Pattern recognition mols  markers encoded in germ line allow cells to be recog, all cells the same in body.. foreigns don’t have same marker  Phagocytic cells- Find and get rid of foreigns Ex) Macrophage,neutrophil ◦Specific immunity(adaptive)- delayed After 5-8 days will go after specific foreigns not gotten by innate to finish job  Can adapt to improve during course of response More ,apid and effective way each exposure  Major components: t & B cells(lymphocytes), antibodies, antigen specific receptors  randomly generated(b & t receptors)... All cells diff so Bind to specific antigens Ex) Humoral immunity- antibodies (b cells) & Cell mediated immunity(T cells)  immune responses tailored to organism involved Intracellular- to get viruses Extracellular- to get bacteria, worm, fungi  Innate and adaptive immunity cooperate ◦Cytokines & chemokines (message) ◦Inflammatory response- brings cells to injured area  Memory = immunity in adaptive  Tolerance- prevent destruction of host tissue ◦Self preservation  Consequence: preservation of cancerous cells ◦If Dysfunctional tolerance --> autoimmunity(attack own body)  Immunity dysfunctions:  Overly active/misdirected response- works as it should but goes too far  Allergy, asthma, anaphylaxis  Autoimmune disease Immu(odeficiency) Primary- genetic loss of immune function (born with)  Secondary- acquired loss of immune function (later in life something happens) Opportunistic infections- caused by microbes that shouldn't usually cause disease Ex) AIDS- lose T cells Ch 2: Cells of the immune system  White blood cells- come primarily from bone marrow in upper leg  Organs ◦primary lymphoid organs (bone marrow, thymus[wbc mature]) ◦Secondary lymphoid organs (spleen[looks in blood and filters worn out rbc, microbes], lymph nodes)  communication happens in middle of body  Blood vessels ◦transfer occurs btwn blood vessels and lymphatic system Lymphatic system Cell types:  Wbc- also called leukocytes ◦neutrophils- predominat wbc... go thru body and make sure foreign things in check- innate system (iis) ◦Lymphocytes- b & T cells- specific immune system(sis) Hematopoietic stem cells(HSCs)- don't wear out and die...regenerate into all diff types of blood cells ◦two diff progenitors- diff'd by ability to regenerate and differentiate ‣ myeloid(bone marrow)  rbc- carry oxygen  Platelets- allow clotting  Granulocytes- have vesicles in cytoplasm w bad chems to release when they find foreign cell needing killed ◦neutrophils- phagocytic, releases granules ◦Basophils/mast cells- help w extracellular infections, worm infections ‣ mast cells release granules with histamine when allergies occur ◦Eosinophils- " "" " " " "  monocytes/macrophages(membrane ruffling from actin fibers extending/retracting) -phagocytic ◦repair/remodel or destroy pathogens ◦Antigen presentation(ACPs)- if cells react then that cell type starts working ◦Exs) osteoclasts(destroy bone), microglial cells, alveolar macrophages(work at lower rate to prevent pneumonia)  lymphoid-  NK cells(natural killer)- act like iis.. Find cancer cells  B lymphocytes- humoral immunity (CD- marker) ◦Activated B cell- has bound to specific antigen, then will differentiate into either: plasma cell- antibody(kind of protein) generating machine with lots more cytoplasm(BC need RNA, Golgi, ER which are all found there) memory b cells- from first exposure to disease so not contracted again ◦B cell receptor(BCR)- all B cells get BCR as maturing many diff options, get one randomly (billions of combos) descendants get same BCR T lymphocytes- cell mediated immunity (CD3+ markers) ◦T helper cell(CD4+)- directors ◦Cytotoxic cell (CD8+)- kill infected cells/pathogens w/vesicles w bad chems ◦Memory dep on cell type ◦T cell receptor(TCR)- all T cells get TCR as maturing ‣ many diff options, get one randomly (billions of combos) ‣ Pos(must recog self 1 to go one)/neg selection(if binds too strong to self, killed)  Bone marrow  B & T cells start in marrow ◦b lymphocytes completely develop here ◦Endosteal niche- quiescent HSCs ◦Vascular niche- HSCs ready to differentiate- T cells escape thru here to thymus t cells have no TCR or CD marker yet Cortex- DP(double positive cell has CD4+ and CD8+) and form TCR(CD3+ marker added) and go through positive selection(should react a little bit to self marker) Medulla- SP(single pos... Loses one(either 4 or 8) marker) and goes through negative selection(cells come to make sure it doesn't react too strongly to self marker) ‣ Mature T cells ready for release  How do lymphocytes get activated?  Receptor TCR & BCR ◦Specific to particular antigen ◦secondary lymphoid organs- communication center and where lymphocytes are activated -lymph nodes, spleen, tonsils/peyer's patches  Connected via blood and lymphatic systems -let out in blood system, move around in tissues, go into lymph system and surrounding skeletal muscles move them to middle of body to show b and T cells(secondary lymph tissues) any antigens Etc found in body  Encounter antigen, initiate immune response Lymph node HEVs(high endothelial venules)- where t and B cells enter lymph node  FRCs guide migration of macrophages and T cells to make sure they encounter all of each other ◦Takes T cell ~1 day to sell all presented antigens on APCs  FDCs guide B cells same way  Spleen: first line of defense(rbc)… defends against blood borne cancers o Rbc in red pulp o Wbc in white pulp o Macrophages & b cells in marginal zone  Malt: o Mucosa- associated lymphoid tissues  For antigens that enter mucosal tissues  Include: GALT & Peyer's patches  M cells in Peyer's patch.. lining of gut- deliver antigen from intestinal spaces to lymphoid cells in gut wall  Immune cells in skin- phagocytose things that shouldn't be there CH 3  Cellular signals- art of detecting and reading ligand(receptor on cell and what it does) o Ligand- soluble molecule released from one cell and picked up by second cell (may travel)  Peptide, carbohydrate, or lipid on cell surface o Receptor alterations(cell #2)- upon ligand-receptor binding, intracellular events take place and change transcriptional program of cell  Interactions:  Weak affinity, but high avidity(overall intxs of cell to receptor)  Multivalency(can bind multiple ligands) increases avidity  If one lets go, another can still be bound so rx will continue o Receptor and ligand expression varies during immune response Ex) activated wbc upregulate receptor for cytokine  Local concentrations of ligands can be very high  Antigen-immune receptor intxs are enhanced by co-receptor binding  Signal transduction pathways- cellular changes that occur during immune response  Upstream- before certain part of process  Downstream- after certain part of process  Internal signaling cascade- changes in transcription(RNA), motility, adhesion  Same ligands can trigger diff receptors in diff cells Receptor conformation changes- 1st step in pathway Antigen-mediated receptor clustering initiates signaling in B and T cells  Lipid rafts- portions of membrane where receptors congregate  Ex) BCR not bound to ligand, outside of lipid raft… when antigen comes in, lipid raft closes  Receptor dimerization- when antigen present(come together)  Multimerization- more than one receptor coming together  Receptor associated mols  B & t cell receptors have short cytoplasmic portions  T cells: use CD3 complexes and CD28 mols  Immuno-receptor Tyrosine Activation Motif(ITAM)- in coreceptors… brings signals into cell  Activation of T & B cells  Src-family kinases- phosphorylate tyrosines  SH2 domains- binds phosphorylated tyrosine  When cell gets activated, kinase keeping other phosphorylated gets activated so other kinase comes in and dephosphorylates it so other becomes active  Adaptor proteins- no enzymatic or receptor function… can bind many things and keep them together in one place  Mediates redistribution of molecules w/in cell  May induce conformational change in one mol  NEED other mols  B cells use Iga(alpha) and Igb(beta) molecules o B cells receptors( Y shape)  Structure of antibody  Immunoglobulin(antibody)- 2 heavy chains and 2 light chains  Variable(pocket where antigen can bind…billions of antibodies. Doesn’t change) and constant region(changes.. varieties: IgA, IgE, IgM)  Disulfide bonds  5 AB(antibody) classes- Differentiated by heavy chain seq…. Diff fxs during immune response  IgM- pentamer… 5 IgM's together, can have 10 diff ligands bound  IgG  IgE- allergies  IgA- mucosal  IgD  Constant domain: Hinge region- keeps arms away so antigen can bind  Variable domains: AB moleule can bind to specific antigen  Each Ab can bind 2 antigens  In membrane until B cell activated  Membrane bound ab has 3 extra regions  Hydrophillic spacer  Hydrophobic transmembrane segment- keeps AB in membrane until b cell activated so it can come out  3 AA cytoplasmic tail  Alternative RNA splicing- makes 1 mRNA and 2 diff types of proteins from it  Signal transduction in b cells  Tyrosine kinase Lyn- gets activated then phosphorylates ITAMS of coreceptors, activating Syk  Coreceptor Iga/Igb  Tyrosine kinase Syk- phosphorylates BLNK adaptor protein  Adaptor BLNK- binds things  …when signaling pathway gets in cell, b cell:  Phosphorylation & inactivation of many cells --> cell survival and anti-apoptotic phenotype (bc cell is needed)  Map kinase activated- growth and proliferation  Transcriptional changes: TF that turn certain genes on/off (NFAT, NF-kB, AP-1) o T cell receptors and signaling( 2 horizontal lines)  TCR similariteis to BCR- Ig domains, variable domains, constant domains  Diff: needs to bind antigen + MHC(self-marker) at same time  TCR heterodimers with alpha and beta chain  Coreceptor CD3 (combo of 6 diff mols..will bind antigen)  CD4/CD8- have immunoglobulin domains  Accessory mols in antigen/MHC binding  Signal transduction in t cells  Tyrosine kinase Lck- binds Zap70  Zap-70- phosphorylates ITAMs  Coreceptor CD3  ITAMs- binds LAT  Adaptor protein- LAT- proteins congregate on it  ...effects: when t cell activated by antigen:  Leads to survival- dec in apoptotic proteins  Skeletal reorganization- changes so can become t cell  Map kinase  TFs: (NFAT NF-kB AP-1)  cytokines- communication marker o secreted from one cell, target cell w cytokine receptor takes it & signals something to happen o Soluble mols- ligand o Interleukins(inter leukocytes)…not all o Chemokines- chemical that induces mobilization of other immune cells to bring them to the cell o Mediate effector functions of immune system  Endocrine action- produced by cell very far from target cell  Paracrine action- nearby target cells  Autocrine cells- target cell is self o 4 diff ways for cell to act on other cell:  Pleitrophy- 1 cytokine can act on multiple cells to do diff things  TH cell(t helper) CD4+… produces IL4: can act on b cell, CD8+ t cell, mast cell, or b cell and cause diff things  Redundancy- 1 cell  CD4+ helper t cell produces 3 IL's that do same thing  Synergy- more than additive, put 2 things together and works much more intensly  IL4 w IL5 causes mass Class switching  Antagonism- can block something  IFN-y can block IL4 o Cascade induction- one thing to few to many to lots o iis(Innate immunity): IL1 & TNF-a: can be made by either type of immune cell but target only iis cells o Sis (specific/Adaptive immunity): IL2 & IL4 (" " " " " ") o What kind of cytokines does the cd4+ t cell make? (Det's cytokines and how response goes from there)  TH17- inflammatory state---> acts on macrophages & neutrophils  IL17  No si cells… majority are ii cells--> leads to massive inflammation  TH1- cytotoxic immune resp ---> acts on macrophagess and CD8+ cytotoxic t cells  Makes IL12 & IFNy  Leads to inflammatory cytotoxic response  TH2- humoral immune system resp---> acts on b cells(make antibodies)  Makes IL4 & IL5  Leads to antibody mediated(humoral) repsonse  Specificity: o Cytokines don’t activate t cells nonspecifically bc:  Activated cell alters cytokine Receptors  Concentrated btwn secreting & target cells  Low half life- just enough to send message  Signaling thru multiple receptors  20 receptors for 50 chemokines  Enzymes diff w/in target cells--> diff downstream events  6 families of cytokines o Based on:  stx of ligand and receptor  Nature of signaling pathways induced  Interleukin 1- Stimulated by viral, parasitic, or bacterial antigens  Pro-inflammatory  Secreted early by macs and DCs(sis)  Acts locally to bring WBCs to infected tissues  Acts systematically to produce fever  IL1- pro-forms(caspase1 activates it by cleaving IL1pro to get IL1)  Binds IL-1R1 & IL-1RAcP receptor in immunoglobulin receptor  Come together in intermembrane region  TIR domains- starts activation of MAPK & NF-kB pathways  MAPK- signaling downstream of ITAMS …cascade pathway… involved in proliferation  NF-kB: TF.. In nucleus, changes transcriptome  Inhibit:  IL1-Ra- binds IL-1R1 and prevents IL-1RAcP from binding so blocks cascade  IL-1R2- binds IL1 in place of IL-1RAcP.. Receptor w/out activation  No TIR domain so signal cant go in cell  IL18- redundant- uses IL1 receptor family and expressed w macs & DCs  Early iis cells  IL-18Ra & IL-18Rb  Inhibited w soluble receptor(IL-1F7 & IL-18BP)  IL33- smooth muscle and bronchial epithelia  Induces TH2 cytokines--> activates B cells and mast cells  Implicated in asthma, allergies, and bowel diseases  Soluble inhibitors  TNF family  TNF-a: proinflamm & produced by activated macrophages & other cell types  TNF-b: from activated lymphocytes  Activation, increased MHC, adhesion  "present more"  Receptors:  Soluble, in memb  Signaling- can lead to many diff things  Fas receptor & Fas-L---> apoptosis & immune system shut down  Fas receptor:  Fas-L interacts w receptor to induce trimerization  Adaptor protein FADD recruited  Binds Fas & makes death domain which activates caspase  Caspase cascade (caspase 8 cleaved to activate procaspase 3 & 7 inactive that activates caspace 3&7)  apoptosis  Hematopoeitin (class 1) family- originate from and affect b & t differentiation, activation, & Ab secretion  IL2- proliferation  Receptors have low/med/high affinity forms  Inacitve- intermediate affinity ( y & b)  NK cells(resting t cells)  Activated- low(a) & high affinity form (y, b, & a)  Activated CD4+ & CD8+ t cells, & activated b cells  Many low affinity, few high affinity…lots of IL2, t cell will bind a lot w low affinity and few w high affinity  Reduces local concentration to keep other inactivated t cells in the area from being unnecessarily activated  IL3/IL5/GM-CSF- antagonism, both signals at same time will inhibit each other  All Binds a subunit, b subunit is shared signal-transducing protein btwn all a chains (usually not enough b chains)  Proliferation unless too much cytokine- saftey mech  Interferon(Class 2) family  Type 1 interferon- a & b  Antiviral affects- Secreted by viral-infected cells(not necessarily WBCs)  If cell 1 infected, can make interferons & secrete so cell 2 picks them up and makes antiviral proteins, so cell 2 can withstand virus & survive  Type 2 interferon- y  Produced from activated T cells & NK cells  Leads to TH1 response(CD4+ T cell)--> cytotoxic/inflamm response  Inc MHC(increased presentation by iis cells) lvls on cells  Intracellular pathogens(viruses, some bac)  IL17 family- pro-inflamm  Expressed by variety of cells  Receptors found on neutrophils, keratinocytes(on skin)  Innate & adaptive immunity boundary o JAK kinase- allow signals to get into cell o STATS- adaptor mols that bring signals further in  Chemokine family- cause mobilization  Secreted by cell , Direct leukocyte migration  Have highly conserved disulfide bonds(lots of cysteine)..very small  Signaling- chemokine receptors help cell move locations  G protein activated- 3 subunits(aby), a dissociated when signal received then binds other mols to move cell  GPCRs- chemokine receptor in membrane


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