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Fate of the Immunogen Equilibrium phase Catabolic decay phase Immune elimination phase • Clearance after 2o exposure – More rapid onset of immune elimination phase Amount of Circulating Ag (%) Clearance after 1o exposure Equilibrium Phase 100 75 50 Catabolic Decay Phase Immune Elimination Phase 25 2 4 6 8 10 12 Days after Injection Kinetics of the Ab Response T-dependent Ag; 1o Response LAG LOG PLATEAU DECLINE Ab Titer • Lag phase • Log phase • Plateau phase • Decline phase Ag Days After Immunization Kinetics of the Ab Response • Lag phase • Log phase • Plateau phase • Decline phase Ab Titer T-dependent Ag; 2o Response 1o Ag 2o Ag * Specificity Days After Immunization Kinetics of Ab Response to T-independent Ags 4 Phases IgM Ab No secondary response Ab Titer IgM antibody 1o Ag 2o Ag Days After Immunization Milestones in immunization 3000BC Evidence of sniffing powdered small pox crust in Egypt 2000BC Sniffing of small pox crust in China 1500BC Turks introduce variolation 1700AD Introduction of variolation in England and later in the US 1780AD Edward Jenner discovers small pox vaccine 1885AD Pasteur discovers rabies attenuated vaccine Edward Jenner Discovery of small pox vaccine Modern era of the vaccine 1920s Diphtheria and Tetanus 1960s Mumps measles and rubella virus Sabin polio 1934 Pertussis 1955 Salk polio 1985 Haemophilu s 1990s Hepatitis and varicella Different modes of acquiring immunity Immunity Innate Acuired Passive Artificial Natural Active Artificial Natural Passive Immunity Natura l Artificia l Placental transfer of IgG Antibodies or immunoglobulins Colostral transfer of IgA Immune cells Passive Immunization disease antibody source indication diphtheria, tetanus human, horse prophylaxis, therapy vericella zoster human immunodeficiencies gas gangrene, botulism, snake bite, scorpion sting horse post-exposure rabies, human post-exposure hypogammaglobulinemia human prophylaxis Active Immunization Natural Artificial Attenuated organisms killed organisms exposure to subclinical infections sub-cellular fragments toxins others Live Attenuated Vaccines polio* not used in std. schedule measles, mumps & rubella Varicella zoster children with no history of chicken pox hepatitis A not required in SC yellow fever Military and travelers tuberculosis not used in this country Recommended Childhood Immunization Schedule (2002) Complement Discovered in 1894 by Bordet It represents lytic activity of fresh serum Its lytic activity destroyed when heated at 56C for 30 min Complement functions Host benefit: opsonization to enhance phagocytosis phagocyte attraction and activation lysis of bacteria and infected cells regulation of antibody responses clearance of immune complexes clearance of apoptic cells Host detriment: Inflammation, anaphylaxis Pathways of complement activation CLASSICAL PATHWAY antibody dependent LECTIN PATHWAY ALTERNATINE PATHWAY antibody independent Activation of C3 and generation of C5 convertase activation of C5 LYTIC ATTACK PATHWAY A damage to host mediated by preexisting immunity to self or foreign antigen Types of hypersensitivity reactions Type I: Type II: Type III: Type IV: anaphylactic or immediate cytotoxic Immune complex cell mediated or delayed Type-I hypersensitivity The common allergy Anaphylaxis can be fatal Sensitization against allergens B cell TH1 Histamine, tryptase, kininegenase, ECFA Leukotriene-B4, C4, D4, Newly prostaglandin D, PAF synthesized mediators Type II hypersensitivity role of neutrophils Complement mediated lysis ADCC frustrated phagocytosis Type II hypersensitivity role of neutrophils B cell TH1 Histamine, tryptase, kininegenase, ECFA Leukotriene-B4, C4, D4, Newly prostaglandin D, PAF synthesized mediators Type III hypersensitivity Serum sickness mediated by immune complexes Type III hypersensitivity mechanism Type III hypersensitivity mechanism Type III hypersensitivity the role of immune complex size Type IV hypersensitivity Delayed reaction 36 to 48 hours Characterized by induration and erythema Also known as cell mediated hypersensitivity Tuberculin test is the most common example Delayed hypersensitivity reactions type time of reaction clinical appearance histology antigen and site contact dermatitis 48-72 hours eczema T cells, later macrophages epidermal: heavy metals, poison ivy, rubber, latex tuberculin 48-72 hours local induration lymphocytes, monocytes intradermal: tuberculin, lepromin, etc. granuloma 21-28 days hardening M, giant cells, epitheloid cells, fibroblasts persistent antigen stimulus, chronic infection Mechanism of damage in contact hypersensitivity M APC TH1 IL2, TNF, IFN IL2 TNF, IFN/ NO2 M NK LAK preTc Tc Comparison of hypersensitivity reactions characteristic Type-I Type-II Type-III Type-IV antibody IgE IgG, IgM IgG, IgM none antigen Exogenous cell surface soluble cellular response time 15-30 min. Min.-hrs 3-8 hours 48-72 hours or longer appearance Weal & flare Lysis & necrosis Erythema & edema Erythema & induration histology baso- and eosinophils Ab and complement PMN and complement Monocytes & lymphocytes transfer with antibody antibody antibody T-cells examples hay fever, asthma pemphigus, Goodpasture farmers’ lung, SLE TB test, poison ivy, granuloma Immunodeficiency Two major types of immunodeficiency diseases Secondary immunodeficiencies immunodeficiency resulting from infections and other diseases immunodeficiency resulting from iatrogenic causes immunodeficiency due to aging or malnutrition Primary immunodeficiency Inherited immunodeficiencies Immunologic defects caused by HIV infection Cellular abnormalities decrease in CD4 T cells (reversal of CD4/CD8 ratio) Functional abnormalities increased susceptibility to infections particularly intracellular pathogens decrease in cell mediated immunity decrease in the NK cell functions Primary immunodeficiency diseases Stem cell defect Reticular dysgenesis T and B cell defect severe combined immunodeficiency X-linked IL2 receptor -chain autosomal adenosine deaminase (ADA) purine nucleoside phosphorylase (PNP)
