• Like
Chapter 21 Immune system
Upcoming SlideShare
Loading in...5
×

Chapter 21 Immune system

  • 712 views
Uploaded on

 

More in: Technology
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
    Be the first to like this
No Downloads

Views

Total Views
712
On Slideshare
0
From Embeds
0
Number of Embeds
0

Actions

Shares
Downloads
8
Comments
0
Likes
0

Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
    No notes for slide

Transcript

  • 1. Chapter 21 Immune system The body’s defenses •nonspecific = innate inherited •vs. any pathogen •always working •local •specific = adaptive = immune developed •vs. specific pathogens •only when stimulated •slower response •memory lines of defense •1st line of defense physical barriers •2nd line of defense internal responses non-specific innate •3rd line of defense immune response specific adaptive 1st line of defense •barriers and secretions •barriers skin mucous membranes •secretions –skin urea , defensins –tears lysozyme –saliva lysozyme –vagina acidic –stomach HCl , enzymes 2nd line of defense •nonspecific responce to presence of pathogens •cell response •antimicrobial proteins •fever •inflammation •cells: •phagocytes macrophages, neutrophils, eosinophils defensins •natural killer cells attack infected cells , cancer cells perforins •antimicrobial proteins : •interferon •interfere w/ virus replication •complement : –classical path Ab-Ag complex cell lysis
  • 2. –alternate path bind to cell wall opsonization inflammation •fever –pyrogens –heat destroys bacteria •increases neutrophil activity •increases interferon production •inflammation inflammation •natural response to injury or infection •prevents spread of damage •removes cell debris •starts tissue repair •signs of inflammation: –Redness (erythema) –Swelling (edema) –Heat –Pain inflammation •chemotaxis cytokines attract WBC to area •leukocytosis WBC proliferation •histamine vasodilation  capillary permeability  swell redness produced by basophils •margination form wall around area (cells + fluid) adaptive (immune) system •3 characteristics : –specific attacks specific pathogen stronger than innate defenses –systemic entire body is immune not just site of attack –memory future responses are stronger who’s who •pathogen foreign cell •antigen (Ag) membrane molecules ID •antibody (Ab) proteins that bind antigens •complement proteins that lyse cells •lymphocytes WBC of immune response •phagocytes WBC that eat pathogens antigens •antibody generators •foreign antigens –cell bound on cell membrane –free toxins –hapten antigenic if bound to host’s protein
  • 3. •self antigens –MHC = major histocompatibility complex –on our cell membranes –used to compare self vs foreign antigens immune cells •WBC - produced in bone marrow •lymphocytes –B lymphocytes mature in bone marrow –T lymphocytes mature in thymus •“mature” - able to recognize a specific antigen •APC antigen-presenting cells –macrophages lymph, connective tiss –dendritic cells connective tiss –Langerhan’s cells epidermis growing up •MHC restriction –positive selection respond to MHC –negative selection strong response to MHC •98% of lymphocytes destroyed •immunocompetent able to recognize foreign antigens –“mature” lymphocytes recognize only 1 antigen •clonal selection proliferation of specific cell clones to fight specific Ag •ability to recognize Ag determined by our genes •which clone is activated determined by pathogen Immune responses •humoral response via fluids –antibodies –B lymphocytes •cell mediated response via cells –cell to cell attack –T lymphocytes B lymphocytes •activated in lymph tissue •antigenic challenge  clonal selection •plasma cells produce antibodies in lymph tissue •memory B cells programmed for future response •
  • 4. •antibodies free floating protein specific for antigen antibodies •immunoglobulins = gamma globulins –IgM early response ; short term –IgG main response ; long term –IgA mucus secretions –IgE allergic responses –IgD B cell receptors •antigen binding site •complement binding site •macrophage binding site •somatic recombination billion different Ab Humoral immune response •B lymphocyte receptors bind with antigen •become plasma cells - produce antibody •antigen-antibody complex •effects: •neutralization inactivates toxins •opsonization stim phagocytosis •agglutination clumping of pathogens •complement stim complement lysis of pathogen •memory cells don’t produce antibody respond quickly to second exposure immune memory •primary response st 1 exposure to antigen –lags 3-6 days –peak about 10 days –rely on non-specific defenses more •secondary response 2nd exposure –faster and stronger response –within hours •memory cells last many years, or for life of individual types of humoral immunity •active immunity –develop memory cells due to exposure •natural exposure to actual infection •artificial “fake” infection = vaccine »killed pathogen antigen still present
  • 5. »attenuated live, weak, pathogen »inactive toxins •passive immunity –obtain antibodies made elsewhere •natural maternal – cross placenta •artificial injection – made in laboratory cell mediated immune response •T cell response •no antibodies •attack –infected host cells w/ foreign Ag –transplanted cells w/ foreign Ag –cancer cells w/ mutated Ag T lymphocytes •helper TH cells CD4 cells T4 cells initiate immune response stim B cell and T cell responses •cytotoxic TC cells CD8 cells T8 cells attack infected cells •memory T cells programmed for future response •suppressor T cells inhibit helper T cells and B cells MHC + Ag •MHC major histocompatibility complex •self antigens •MHC I on all body cells –MHC I + Ag activates TC •MHC II on immune cells –MHC II + Ag activates TH •TCR T cell receptors Ag specific initiation •APC engulf pathogen •travel to lymph tissues •APC’s activate T helper cells •present Ag + MHC II •TH w/ TCR responds TH activate other cells •cytotoxic T cells •B cells •all Ag specific TC cell responses
  • 6. •attack body cells w/ Ag + MHC I •bind to infected cells •perforins lyse cell membrane other T cell responses •suppressor cells inhibit TC and TH –after Ag destroyed –inhibit or destroy T cells •memory T cells TC and TH problems of self antigens •tissue typing ABO , MHC –compare donor tissue and recipient tissue •organ transplants •autoimmune diseases –faulty MHC and/or T cell recognition –Rheumatoid arthritis synovial lining –Multiple sclerosis myelin axons –Myasthenia gravis Ach receptors –SLE (Lupus) connective tissues, DNA –Type I Diabetes beta cells –ankylosing spondylitis vertebral c.t. hypersensitivity •over-reaction of immune response – damages tissue •allergy IgE and Mast cells huge histamine response –asthma inhaled allergen •anaphylaxis (anaphylactic shock) –extreme response to allergen –if systemic : swelling of all tissues •closure of bronchioles can’t breathe •loss of blood volume circulatory shock •death immunodeficiency •immunodeficiency - failure of immune response •Hodgkin’s disease cancer of lymph nodes •HIV = human immunodeficiency virus –attacks T cells (helper T) –blocks CD4 receptors –retrovirus •makes DNA from RNA reverse transcriptase •AIDS = acquired immune deficiency syndrome –HIV positive plus symptoms –infections , malignancies