Immunity Innate & Adaptive
Immunity Innate: response to attack is always the same Mechanical mechanisms Chemical mediators Cellular response Inflammatory response Adaptive: response to attack improves with each exposure Specificity Memory
Innate immunity Mechanical mechanisms Physical barriers prevent entry Skin & mucus membranes (Verts) Chitin exoskeleton (Arthro) Dilution of invading army of pathogens & wash away pathogens from surface Tears, saliva, urine
Chemical mediators Innate immunity Some prevent entry to cells, kill bacteria, produce inflammation 1. Complement proteins ~ 20 in plasma normally inactive; activated by combining with parts of bacterial cells or antibodies Leads to chain rxn activation of neighboring compliments & inflammation, phagocytosis, and lysis
Chemical mediators Innate immunity 2. Interferons protect against viral infection Virus-infected cells release interferons (SOS signal) Some bind to neighboring cells & stimulate neighbors to produce & secrete antiviral proteins Intiviral proteins inhibit production of new viral RNA Some interferons activate macrophages and NKC Low ph digestive sac digests some cells walls
Cellular mechanisms Innate immunity White Blood Cells (Leucocytes) are most important cellular components Attracted to invading bacteria and microorganisms through chemotaxis Phagocytic cells Inflammatory cells Natural Killer Cells (NKC)
Large; contain nuclei Travelers in blood; wandering militia Distributed (via blood) to body tissues where they leave bloodstream and crawl around 2 Jobs 1. Remove dead and dying cells via phagocytosis 2. intercept & destroy invaders Leucocytes
Innate immunity Phagocytic cells Neutrophils Small; first to enter infected tissue from blood; ingest, then die --> pus accumulation Macrophages Monocytes leave blood & enlarge; arrive after neutrophils; do most eating & cleanup Also hang out at entry points (gate-keepers)
Innate immunity Natural Killer Cells (NKC) 15% of all lymphocytes are NKC Recognize tumor cells or virus-infected cells (generalist killers) No memory; non-specific Kill via chemical release (perforins lyse cell membranes)
Innate immunity Inflammatory cells: activated through innate or adaptive immunity; release histamine & such Basophils Motile WBC; enter infected tissue Mast cells Non-motile; Located in CT at points of entry Eosinophils Release enzymes that reduce inflammation (control)
Innate immunity Local inflammation Redness, heat, swelling caused by increased blood flow and vascular permeability Chemicals and swelling activate pain receptors (what type of receptors are these?) Systemic inflammation Red marrow increases neutrophil production Pyrogens stimulate fever by increasing heat production & conservation Vascular permeability increases (why?)
Coordination of innate responses Inflammation, chemotaxis, phagocytosis
Adaptive immunity Lymphocytes Origin & development Activation & multiplication Antibody-mediated Cell-mediated
Adaptive immunity Antigens stimulate adaptive immune response Self Foreign MHC molecules display antigens Lymphocytes Origin & development Activation & multiplication Types of Adaptive Immunity Antibody-mediated B cells; produce cells that make antibodies Cell-mediated T cells; cytotoxic (T c ) & helper (T h )
Foreign Antigens Unique components (proteins or polysaccharides) of bacteria, viruses & their chemical byproducts Pollen, hair, foods are antigens that can produce allergic response (overreaction of immune system) Self Produced by our bodies Used to recognize tumor antigens
Cell Development Red marrow produces: Pre B-cells: released into bloodstream and migrate to lymph organs Pre T-cells: migrate to thymus & mature there Mature T-cells migrate to lymph organs
B & T-cells Contain unique antigen receptors in their cell membranes We each have thousands of different populations of B & T- cells, each with unique antigen receptors Cells are stimulated by binding of antigens to their unique receptors
How are antigen receptors created? 1 receptor gene contains many repeats Recombinase randomly joins V & J segment, & eliminates intervening sequence Alternative splicing creates enormous diversity in variable binding sites 1 gene codes for potentially 1000 s of receptors
MHC molecules display antigens MHC I: displays antigens on infected cells All nucleated cells can do this T c cells bind & respond by killing cell with perforins
MHC molecules display antigens MHC II: displays antigens when a cell phagocytizes a pathogen (APC cells) Only phagocytic cells do this T c cells bind and autostimulate T h cells bind & stimulate T c & B cells & autostimulate
B cell activation Antibody-mediated B-cells can also phagocytize & process antigens same antigen that stimulated a T h T h binds to B-cell Interleukins are produced stimulate B-cell division & proliferation Daughter (plasma) cells produce antibodies
Once B and T h cells are stimulated, they produce two cells types Plasma produce antibodies Memory hang out & remember B-cell proliferation
Effects of Antibodies Direct: Antibodies bind antigens = inactivation Indirect: Activate Complement cascade Series of proteins that stimulate innate immune responses: Inflammation, Chemotaxis, Phagocytosis or lysis
Differs following first and second exposure to antigen Antibody production First exposure = primary response B-cells bind antigen; produce plasma cells (produce antibodies) and memory B- cells Response time = 3-14 days; disease symptoms develop; SLOW
Second exposure = secondary response Memory cells quickly produce plasma cells and antibodies Shorter lag time More plasma cells & antibodies produced RAPID response precludes disease symptoms = immunity Antibody production
T h cell help adaptive immune response APC ingests, processes & displays antigen T h binds, autostimulates & stimulates B & T c cells
APC, T h, T c & B cells Humoral response
T c contact-kill infected cells Cellular response Perforin & granzymes digest infected cells
T cell responses
Show Immune Response
Acquired immunity