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