immune system
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TRANSCRIPT
Immunity
Nonspecific Defense
Skin and Mucous Membranes
• acid sweat pH 35
• 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 livedamoeboid cells - ingest bacteria, viruses, and cell debrissome bacteria have defenses to these
eosinophils - cytoplasmic granules with enzymes used against invaders – dischargedmainly 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 immunitysome serve as memoryno 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 activatedcommon 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