Immunity

Immunity Nonspecific Defense Skin and Mucous Membranes • acid sweat pH 35 • enzyme in perspiration, tears, sweat, and saliva • lysozymes - attacks bacterial cell walls • respiratory tract contains cilia and mucus • digestion - acid in the stomach Leukocytes • neutrophils - chemotaxis - attracted by chemical signals – self-destruct when destroying others – few day life span • monocytes - morph into macrophages: longer lived amoeboid cells - ingest bacteria, viruses, and cell debris some bacteria have defenses to these eosinophils - cytoplasmic granules with enzymes used against invaders – discharged mainly attack parasites (worms) natural killer cells - kill off infected cells of own body - very versatile in what attack – – – – recognize new/unusual proteins on the plasma membrane more rapid response than other cells may stop tumors and virus infestations poke hole in plasma membrane - proteins called perforins plasma cells - produce Ab that are in blood Antimicrobial Proteins • complement proteins that ID and dagger invaders – interact with other defense mechanisms Antimicrobial Proteins • interferon - virus infested cell (and activated lymphocytes and macrophages) – releases substances that will improves nearby cell defenses – increase protein production that inhibit viral replication – especially for short term infection - cold and flu – activates phagocytes Interferons Inflammatory Response - pain, heat and swelling • • • damaged cells release prostaglandins, proteins, and K+ vasodilation increase blood supply histamines released (from mast cells or basophils) cause localized vasodilation – prostaglandins also help this to happen heparin reduces clotting so new cells keep coming and cleansing – later a clot forms to seal off and slow spread of pathogens increased temperature (increased blood flow) - activates/catalyzes enzymatic reactions of phagocytes – may also denature foreign enzymes or proteins phagocytic cells migrate to area - via complement proteins and other factors – 1st = neutrophils: activation - increased metabolic activity – release H2O2 and nitric oxide to kill of pathogens – invade then die macrophages remain to protect – may get pus from dead cells and fluid during clean up – severe infection  systemic response – bone marrow releases more neutrophils – increase leukocytes fever - due to pathogens or proteins called pyrogens that re-set temp for battle • • • • • Lymphatic System - tissues and free cells • Cells = T cells (thymus-dependent) cells, B cells (bone marrow derived) and Natural Killer cells • lymph node = lymph tissue wrapped in fibrous CT • percolate out unwanted - capture cancer cells Temperature • • • • fever - stimulates phagocytosis inhibits microbial growth reduces Fe that bacteria need speeds up tissue repair Specific Response • T Cells – start in bone marrow  thymus where mature – Cell mediated response – ID via antigens produced – Several kinds of effector cells – Helper - initiate humoral and cell mediated response – stimulate activation of both T cells and B cells – Cytotoxic - lyse cell infected w/ virus or cancer production of cell mediated immunity some serve as memory no response on first exposure, but many made for next time Natural Killer cells = lymphocytes – surveillance of cells – attack foreign cells, viral infected cells and cancer cells – Inducer – development of T cells in thymus B Cells - bone marrow – Humoral response or Ab response – ID antigen and the start to reproduce --> plasma cells (= effector cells) – which secrete Ab’s that flag antigens for destruction • • Strategies • Innate immunity - genetically determined – people not susceptible to same diseases as gold fish • Active immunity - after exposure to an antigen – own immune system - has many capabilities these are stimulated after exposure • Natural from infection - starts to develop after birth – develops on an as needed basis • Artificial (Induced) - deliberate exposure – from vaccination/immunization – and the forced version: where your Mom forced you to play with the kid with chicken pox so you could develop immunity • Passive immunity - Ab from one individual to another – usually short lived – example mother to fetus - across placenta, in milk – can also be artificial (induced) Humoral response • Ab immune response to toxins, bacteria, and viruses – Ab production from lymphocytes, carried on B cells plasma membrane – if antigens bind to Ab then the B cells are sensitized – sensitized B cell encounter an already activated helper T cell – B cells then usually --> mitosis --> plasma cells and memory B cells • Memory B cells --> 2nd exposure --> mitosis Ab aid to destroy antigens – Neutralize - land on specific site on pathogens needs to enter host cells Ab aid to destroy antigens – Agglutination and precipitation - form bridges between two pathogen cells – Ab can bind on two spots - tips of Y Ab aid to destroy antigens Activate complement when bound to antigen change in shape so compliment proteins bind complements = proteins that supplement the action of Ab’s destroy target cell’s plasma membrane - create a pore Ab aid to destroy antigens • stimulate inflammation - basophils and mast cells • attract phagocytes - neutrophils and macrophages • makes target easier for macrophages to engulf • gives phagocytes something to hang onto vs slick cell membrane of some bacteria • Attract phagocytes - eosinophils, neutrophils, macrophages • Prevents bacteria and viral adhesion • makes it hard for pathogens to attach Cell mediated response • • • • • • • • • • attack viruses, abnormal cells, bacteria, fungi, protozoans, worms, transplant tissues, cancer cells – T cell activation - before immune response must activate by exposure to antigen Major histocompatibility complex (MHC) glycoprotein self markers unique to each individual MHC Class I: membranes of all nucleated cells, from golgi if abnormal peptides are present  T cell activated common for viruses to bind here MHC Class II: found only in Antigen presenting cells – = all monocytes/phagocytes = microglia, in CT, in liver T cells are specific to an antigen - only activated to certain antigens Memory - based upon memory cells from 1st infection 1st immune response = increase lymphocytes to form clones of effector cells 2nd immune response = faster, Ab more effective at binding to antigen from second time infected