Bacterial diseases Pneumonia Gonorrhea TB Legionnaires Strep throat Athelete’s foot Jock itch Vaginal yeast infections thrush Malaria Sleeping sickness Pinworm Intestinal roundworm AIDS Polio Chickenpox Smallpox Measles, hepatitis, herpes, mono, flu Alpha 1, alpha 2 = peptide binding part Beta-2-microglobulin doesn’t cross membrane CD8+ T cells  cell death Binds 8-10 AA peptides (ends in pockets) Endogenous (cytosolic) pathway for Ag Alpha 1, beta 2 = peptide binding CD4+ T cells  recruitment Binds 12-20 AA peptides Exogenous Ag T cell (TCR) APC/Target (MHC) CD4 MHC II CD8 MHC I LFA-1 ICAM CD2 LFA-3 CD45 CD45L CD45 CD45L CD3/zeta-zeta CD28 B7 (CD4 and 8) 4-1BB 4-1BBL (CD8) Binds B7  inhibitory signal Activated T cells Resting T cells IgG, IgD, IgE IgM (has J chain) IgA (has J chain) Ag + BCR complex  signal transduction (kinases)  activated B cell  blasts OR memory cells: Blasts  plasma cells in marrow  Ab Somatic hypermutation Class switching Memory Contact help, cytokine help APCs for TH: DCs (early attack); B cells (late attack) Crosslinking Large multivalent Ag (eg. LPS) Predominant Ig secreted with T-ind = IgM Little, no memory

Fungal infections Parasitic diseases

Viral diseases

Class I MHC

Class II MHC

Coreceptors Adhesion molecules Signal Transduction Costimulation CLT4-A CD45RO+ CD45RA+ Monomeric Ig Pentameric Ig Dimer B Cell Activation

T-dependent Ag

T-independent Ag


Haptens CDR3 RAG proteins Ab forms of diversity TCR forms of diversity Diversity for both Abs and TCR AID PALS (spleen) Follicles (spleen and lymph nodes) Marginal zone (spleen) Lymph nodes – cortex Lymph nodes – paracortex Lymph nodes – medulla T cell maturation B cell maturation AIRE Peripheral tolerance – T cells Peripheral tolerance – B cells Addressins Selectins. cleavage. if k not made. VDJ recombinase for TCR) Junctional diversity (CDR3 for TCR) Deletions. B and T. k or L. then lambda is  IgM  immature B cell in marrow  blood  spleen  mature Central tolerance Causes expression for tissue-specific Ag – allows for negative selection of T cells Mature T cells that bind self Ag in periphery Anergy: signal 1 (TCR engaged) but no signal 2 (B7 costimulator) Suppression Apoptosis: no costimulator  Fas and FasL on CD4+ (death receptor)  caspases  death B cells bind T-dep self Ag -> anerg CD34 GlyCAM-1 On HEV L-selection adhesion receptor On B/T cell Survival signal to B cells to go to follicles B cells in marginal zone of spleen for T-ind Ag Secondary have germinal centers No BCRs. death)  light chain. ligation (Rags. insertions N region addition (TdT) Reading of D in all frames Random chain association Mediates somatic hypermutation: deaminates C to U T cells B cells Lymphocytes and macrophages B cells T cells Macrophages. integrins (homing receptors) BAFF MZ B cells Primary vs. Secondary follicles NK cells Opsonins Effector functions Small epitopes that bind BCRs Not immunogenic Hapten-carrier conjugate can form peptides and present to T cells on MHC II Responsible for junctional diversity for TCR Recombination-activating genes for VDJ recombinase Somatic hypermutation Class switching (H chain) Occur in peripheral organs D-D or skip joining Combinatorial diversity Alignment. no TCRs NKT cells – have TCRs of restricted diversity Agents that promote phagocytosis of Ag by binding and coating Ag IgA and IgG Phagocytosis Cellular cytotxicity (Ab) Complement cytotoxicity (killing via soluble component) Inflammation Ic clearance 2 . plasma cells Beta chain rearrangment in double negative thymic cells in thymus  make functional beta chain (allelically exclusive) w/ pTA (= preTCR)  alpha chain rearrangement (not exclusive) and CD4/8 expression (double +)  alpha/beta TCR binds self MHC  diff into CD4/8+ Progenitors in marrow  pro B cells  H chain rearrangement (mu)  pre-B cell (have H chain)  pre-BCR (2 mu. no BCR.

Cytotoxic NK cells Eosinophils Monocytes/macro/neutrophils Inflammation Mast cells and basophils Lipid mediators for mast/baso Cytokines Immune complex clearance Classical complement path (Ag/Ab activated) NK cells Eosinophils Monocytes/macrophages. ADCC (IgA. C3a. E) Fc-epsilonRII on eosino binds Fc of Ab Granules (MBP) released  kill Exocytose Macrophages carry out ADCC (via IgA. IgA No Ag-specific receptors aR (on NK) binds CHO  kills iR (inhib) binds MHC I  protective ADCC (NK kill Ab-coated target) Kill worms Innate. and predominant in blood Opsonin Classical comp ADCC Trans-placental Neutralization 3 . proteases PAF Thromboxane Prostaglandin Leukotrienes IL-4  class switching to IgE  activates mast cell TNF  activates mono/macro  Ag clearance Opsonization (Phago) Transport to spleen via classical complement pathway (RBC) Endo/degrade (B cell) C3b and C4b bind CR1 on RBC  spleen  Ag/Ab clearance (major route) C3b. neutrophils Kill tumor and infected host cells IgG. C4a (anaphylotoxins) Mannan-binding lectin path Alternative pathway Soluble regulators of complement Membrane regulators IgM IgG C5-9  cytotoxicity Not Ag/Ab activated Protease activation: MASP 1. C4b bind CR1 on B cells  endocytosis  degraded  peptide/class II display on B cells and macros Inflamm mediators: C5a. 2 Not Ag/Ab activated Directly on Ag surface: C3b bidns Ag  Factor B Inflam and opsonin C1Inh Factor 1 S protein CR1 DAF HRF and CD59 Sialic acid Major in blood Classical comp Neutralization Major in EC space. G. IgG) Mast cells and basophils IgE (binds FcepsRII on mast/baso) IgE crosslinking  release Histamine (dilation).

IgE IgA 4 signs of inflammation Main cytokine producing cells Cytokine inhibitors Anti-viral Pro-inflammatory Immuno-modulatory Promoting growth and differentiation of immune cells Chemo-attractants Immuno-suppressive IL-1 IL-2 IL-4 IFN alpha/beta (type 1 interferon) IFN gamma (type 2) TNF-alpha and TNF-beta Skin. mono. pain Macro/mono CD4+ T cells IF-gamma (antagonize) TNFBP (truncate) IL-IRA (competes) CYTOKINES IFN-alpha IFN-beta IL-1 TNF IL-6 (acute phase prot) IL-17 (leuko recruitment) IL-2 IL-4 IFN-gamma G-CSF (neutro) GM-CSF (macro) M-CSF (mono) IL-3 (hemato stem cells) IL-7 – T/B maturation Epo BAFF – survival of B cels CC chemokines (MCP-1) – attract mono/T cells CXC chemokines (CXCL8) – attract neutro IL-10 (on mono/macro) IL-4 (on mono/macro) TGF-beta (on lympho. macro) Pro inflammatory Pyrogen Made by: mono/macro Stimulates IL-1. swelling. NK cells (cytotoxic) Pro-inflammatory Made by many cells Activates mono/macros 4 . submucosal Inflammation (sensitization of mast/baso) ADCC Main one in body/mucosal secretions Opsonin Trans-epi transport Neutralization ADCC Redness. enhances NK cytotoxicity Immunomodulatory Made by: TH Blocked by IFN-gamma Induces class switching to IgE and B cell prolif Anti-viral Made by almost all cells Inhibits viral replication Immunomodulatory Made by: T. IL-2 production Immunomodulatory Made by: CD4+ T cells Is growth factor. NK cells Antagonizes IL-4 so inhib class switching Activates macros. heat. TNF.

macro Made by T cells Made by various cells Made by kidney and liver cells Made by T cells Made by thymic and marrow cells Made by many cells  induce granule exocytosis with inflam mediator release and upregulation of adhesion molecules Suppresses immune function against flora IFN-gamma Macro activation TNF Cytotoxic (Fas) IL-2 CTL activ Switch to IgG IL-10 Ig prod (B) IL-4/13 Switch to IgE IL-5 Eosino/mast cell activ Cross microbes from apical to basolateral aspect in gut HIV – CD4 (on TH) Influenza – sialic acid (on host) Rhinovirus (ICAM-1/2) Physical Chemical Mechanical Normal flora IgA (sIgA has secretory component that prevents microbe from attaching to host. RNA helicases. complement) IFN alpha/betta and IFN-gamma Apoptosis of PRR cells (TLRs. NOD. C3a) Mast cell (histamines. scavenger receptors) Cytokines from macro and NK (lots of TNF-alpha. excreted) Intraepi (CD8+ T cells) Subepi lymphocytes Macros IgE mast cells Dendritic cells Complement (C5a. mono. eosino. prostacycline) Dendritic cells (Ag presentation. chemokines) Endo cells (NO. go to periph organs) Phago (macro. CRP) CMI (CTLs. IL-1 = septic shock) APRs (SAA.TNF inhibitors BAFF CSFs G-CSF GM-CSF M-SCSF Epo IL-3 IL-7 Chemokines Th3 Th1 (inflammation) Th2 (worms) M cells Known host receptors First barriers to infection Second barriers Inflammation Innate immunity Adaptive immunity Extracellular bacteria Intracellular bacteria Fungi Direct tumor killing Pyrogens Stimulate expression of adhesion molecules Anti-TNF Ab Soluble TNF receptor B cell activating factor Made by: dendritic cells and macros B cell survival in follicles Inflammation  enhanced CSF production Made by T cells. CD8+. IL-1. neutro) Cytotox (NK. mono. proteases) Macro (TNF-alpha. CD4+) Humoral Humoral (IgM) CMI (Th1 CD4+) Leprosy determined by Th1 or Th2 type CMI + humoral 5 .

eosino) Humoral (early). heat stable. CMI (after host invaded) CRP (opsonin) SAA (ox burst. need booster) Subunit vaccines – dead. botulinum (exqotox) Systemic inflammation caused by large increase in TFN-alpha and IL-1 Contains Ag-specific Ab Direct Ab source Precipitin curve Nephelometry – measure Ag concentration by adding known Ab concentration Soluble Ag Insoluble Ag Hemagglutination (titer) Enzyme label for immunoassay (HPO) Conversion of added substrate to color – more free ligand  more color Pregnancy tests Radioactive isotoe label Fluorescent label SDES-page (detergent used on Ag) Obtain info on single cells in population Plot as histogram: cell number vs. allergy IgE Ag-Ab (min-hr) Hay fever. inhib platelet activation) Initiators = LPS (endotoxin). induce immunity to disease not toxin Rotavirus MMR Polio (oral) Varicella Hep B Rotavirus Diptheria-tetanus-pertussis H. weakened Ag) Whole microbe inactivated dead (non-rep.Protozoa Worms Viruses Major APRs Septic shock Anti-serum Immunoprecipitation Agglutination ELISA RIA IFA Western blot Flow cytometry (FACS) Immunohistochemistry Direct immunoassay Indirect immunoassay Clinical trials Passive immunobiologics Active immunobiologics Live vaccines Childhood immunization Type I hypersensitivity CMI + humoral (IgG) Humoral (IgE. food allergies = local reaction Anaphylactic shock = system reaction Allergen + IgE  activate Th2  mast and basophil degranulation  inflammation Detection: RAST (meas. fluorescent intensity Ab labeled with enzymes Same as immunofluorescence Primary Ab binding to Ag Secondary Ab binding Ag. asthma. only parts of microbe Toxoids – dead. Skin test 6 . influenzae Inactivated polio MMR Varicella Meningococcal Penumonococcal Influenza HepA HPV Anaphylaxis. more sensitive I – safety II – high-risk groups III – randomized IVIG (intrave Ig) Attenuated vaccine (live. IgE).

Type II hypersensitivity Type III Type IV Transplantation stages of rejection Hyperacute Acute (cellular) Acute (vascular) Chronic Dendritic cells Organ transplant Bone marrow transplant Tissue typing: Serological test One way MLR Oligomer typing assays Cross matching Generalized immunosupression Therapy: avoidance. OKT3 7 . rheumatoid arthritis Detection: skin tests with Ag – tuberculin. hemolytic disease (Erhtryobastosis fetalis). systemic lupus Detection: immunofluorescence (granular. CTL (CD8+). Ab for bacteria. gancyclovir for viral. acute. autoimmune disease Detection: Coombs (IgG anti-RBC Ab hemaggglutination assay) Therapy: diuretics. IgG Ag-Ab (min-hr) Ag + IgM. chronic Type II hypersensitivity Min-24 hours post transplant Caused by Ab Type IV 10 days – few weeks post Caused by T cell Type II Days to months post Caused by Ab Type III. hydrocortisone for contact derm Hyperacute. IV Months to years post III caused by Ab IV caused by T cells Most potent stimulators of allogenic reactions Host vs. lumpy bumpy) on biopsies Therapy: serum sickness – heparin. ADCC  cell killing Transfusion reactions. TDTH TCR/MHC-Ag (24-72 hr) Microbe  TCRs. patch Therapy: eliminate Ag. opson. UV. IgG Ag-Ab (min-hr) Local (zone of equiv)  classical comp  comp clearance Systemic (Ag excess)  inefficient comp  difficult clearance  complex accum on BM/inflammation Arthritis. memory Ag-spec cells  inflammation delayed Contact dermatitis. corticosteroids Immune complex Soluble Ag IgM. IBS. hyposensitization Ab-dependent cytotoxic Insoluble Ag IgM.G  classical comp. SLE (lupus) – corticosteroids) Delayed type (DTH) Peptide Th1 (CD4+0. host Recipient WBC + anti-HLA antisera Typing B cell + test leukocytes Testing for ability for typing B cell to stimulate cell prolif of test WBC pop PCR – detect HLA allele differences Determine whether recipient serum has Ab that react with WBC of donor Match at HLA loci – six Ag match. MMF) More selective: ALG. serum sickness. graft Graft vs. always match ABO and Rh Most important for bone marrow transplants Corticosteroids (prednisone) Anti-mitotic drugs (azathiprine) Xenobiotics (cyclosporine A.

protease. CNS) – trt = IFN-beta Rheumatoid arthritis (women > men) = trt = anti-TNF-alpha Systemic lupus (women > men) Molecular mimicry Polyclonal B/T cell activation Preferential Th1/Th2 activation (cytokine imbalance). maro Surgery  radiation  chemo Immunotherapy: passive (admin Ab). gp41 fusogenic) Pro (RT. genetic. NKT (TCR expressed towards alpha-gal-cer on cancer cell). IFN-gamma LAD (integrin beta chain defect. gut Trt = marrow transplant Chemical carcinogens Ionizing radiation Oncogenic viruses Sarcomas (mesenchyme) Lymphomas Myelomas (plasma cells) Leukemias – single cell cancers Carcinomas (epi origin) CA125 – ovarian cancers Glycoport and glycolipids that differ in cancer cells Her-2 – breast cancer CEA – colorectal cancer CD8+ . NK. impaired CTL) Gag (p24 core prot) Env (gp120 attachmt. integrase) Rev (regulates viral exp) Tat (transcription activator) ELISA or Western blot (detect anti-HIV Abs). Xlinked. HLA alleles) AIRE gene defect Affects endo gland FoxP3 defect X-linked Endo glands. if Th1 = excessive IR Epitope spreading Injury Predisposition (gender.M) DiGeorge syndrome Trt = bone marrow transplant X-linkedd SCID Trt = bone marrow ADA Zap-70 deficiency CGD (X-linked) Trt = prophylactic Ab. PCR (proviral DNA) 8 . low IgG.A. active (immunize) XLA Trt = IVIG Hyper-IgM syndrome (CD40L defect.Ag-specific Autoimmune diseases to know Development of Autoimmunity APD IPEX Malignant tumor causes Cancer types Tumor specific Ag (TSA) Tumor assoc Ag (TAA) Immune responses against cancer Cancer therapies B cell deficiencies T cell deficiency T and B cell def Phagocyte deficiency HIV genes HIV regulator prot HIV detection Blood transfusions Soluble CTLA-4 with recipient WBCs Pretreat graft with anti-lympho Ab or anti-HLA Ab Ankylosing spondylitis (Ab to vertebral Ag) Autoimmune myocarditis (Ag post heart attack) Grave’s (women > men) Hashimoto’s (women > men) Ins dep diabetes (panc beta cells Ag) Multiple sclerosis (women > men. CD4+.

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