2. Ch 31 immune system AP lecture

3. http://highered.mcgraw- hill.com/sites/0072507470/student_view0/ch apter22/animation__the_immune_response.h tml http://highered.mcgraw- hill.com/sites/0072507470/student_view0/ch apter22/animation__the_immune_response.h tml

4. Immunity The ability to avoid disease when invaded by a pathogen Animals have two ways –Innate immunity – nonspecific First line of defense Second line of defense –Adaptive immunity – specific Involves antibody proteins Only vertebrates

6. White blood cells Phagocytes- engulf pathogens –Innate and adaptive Lymphocytes –Adaptive

7. Innate, nonspecific defense 1 st line: –Skin –Salt concentration on skin –Normal flora –Musuc –Lysozyme –Defensins –Internal condition

8. 2 nd line of defense –Phagocyte activation –Natural killer cells –Complement proteins One protein binds to invading cell and helps phagocyte recognize and destroy cell Other protein activates the inflammation response and attract phagocytes to site Other proteins lyse the invading cell –interferons

9. Inflammation Bodies response to damaged tissue, causes redness, swelling and heat near the damaged tissue –Isolates damage, stops the spread –Promotes other cells to help with healing –First response mast cells Adhere to skin and lining of organ and release chemicals

10. –Tumor necrosis factor- cytokine that kills target cells and activated immune system –Prostaglandins- initiate inflammation in nearby tissue –Histamine- increase permeability of blood vessels to white blood cells so they can act in nearby tissue

11. Redness and heat caused by dilation. Phagocytes and neutrophils responsible for healing associated with inflammation. Also produce cytokines that signal the brain to produce fever. Rise in body temp causes increased production of phagocytes and lymphocytes – speeding up the immune system.

13. Medical problems- sometimes too strong –Allergic reaction –Autoimmune disease – no recognition between self and non self cells –Sepsis – inflammation do to bacterial infection that does not stay local.

14. Adaptive players 1. Antibodies – proteins that bind to substances identified as nonself -Inactive or destroy pathogen -Tag for immune system to attack -Produced by B cells

15. 2. major histocompatibility complex –MHC I- found on the surface of most cells Present antigen to T C cells –MHC II- found on most immune cells Present antigen to T H cells –Coordinate interactions between lymphocytes and macrophages

16. 3. T cell receptors – integral proteins –Expressed on T cells –Recognize and bind to nonself cells presented by MHC proteins

17. 4. Cytokines- soluble signaling proteins –Bind and later behavior of the target cell –Activate or inactive B cells, macrophages and T cells

18. Adaptive immune response key features –Specific – pathogen present –Diverse- respond to several pathogens –Identifies self from non self –Immunological memory – more efficient when pathogen present again

19. Specificity –B and T lymphocytes –B cells make proteins and T cells that bind to antigens (non self substances) –Initiates immune response –Antibodies react with antigenic determinates (sites on antigen)

20. Diversity –Need for a wide range of lymphocytes for all the pathogens that can be encountered

21. Self from non self –Should recognize self –Failure leads to autoimmune disorders

22. Immunological memory –Immune system can remember pathogens and respond more rapidly – primary response take several days to produce antibodies and T cells –Memory happens because lymphocytes divide and differentiate into Effector cells Memory cells

23. Effector cells –Only live a few days –Carry out attack on the antigen –Effector B cells and plasma cells secrete antibodies –Effector T cells release cytokines to destroy non self

24. Memory cells –Have ability to start dividing on short notice –Produce effector and more memory cells –Memory B and T cells can survive decades in the body Principle behind vaccinations

25. Three phases of adaptive immune response –Recognition- self or non self –Activation- fight the invaders –Effector- destroy the invaders Two types of adaptive immune response –Humoral immune response – B cells –Cellular immune response – Tc cells and cytotoxic T cells

26. Humoral Immune response Recognition is when an antigen binds to a B cell holding the antibody specific to that antigen Antibodies

27. Two regions –Constant region General structure and function When acting as a B cell receptor, this part inserts into the membrane –Variable region Different for each specific antibody Antigen binding site Bivalent: two antigen binding sites; forms clusters and makes for easier ingestion by phagocyte.

28. s s s s s s s s s s s s s s s s s s s s s s s s s s s s s s s s s s s s Structure of antibodies light chains antigen-binding site heavy chains antigen-binding site light chain B cell membrane heavy chains light chain variable region antigen-binding site Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y

29. macrophage plasma cells release antibodies Y Y Y Y Y Y Y Y Y Y Y Y Y B cell immune response tested by B cells (in blood & lymph) 10 to 17 days for full response invader (foreign antigen) B cells + antibodies Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y recognition Y Y Y Y Y Y Y Y clones 1000s of clone cells Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y memory cells “reserves” Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y YY Y Y captured invaders

30. Cellular immune system Recognition when an antigen is inserted in the plasma membrane of an antigen presenting cell. Antigen is then recognized because it matches the T cell receptor on a T helper (T H ) cell B cells binds to antigenic fragment that has been ingested, so T H cell binds to B cell T H cell stimulates B cell to divide and make clones and activates the adaptive immune response

31. T H cell binding to antigen presenting cells also releases cytokines that stimulate the cytotoxic T cell (T C ) with the same T cell receptor to divide So we have Clone of B cells with specific antibody against antigen clone of T C cells that can bind to the antigen Trying to eliminate the antigen presenting cell (target cell)

32. T cell response stimulate B cells & antibodies Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y YY Y Y killer T cell activate killer T cells or interleukin 1 interleukin 2 helper T cell recognition clones recognition APC: activated macrophage APC: infected cell

34. Tregs- regulatory T cells –Make sure immune response does not get out of control –Made in thymus –Express T cell receptors –Activate when bound to antigen MHC complex –BUT the antigens they recognize are self antigens –Release cytokine interleukin 10 which blocks T cell activation and leads to apoptosis of T C and T H cells

35. Immune response free antigens in bloodantigens on infected cells humoral responsecellular response B cellsT cells macrophages (APC) helper T cells plasma B cells memory B cells memory T cells cytotoxic T cells Y Y Y Y YY Y Y antibodies Y Y Y skin pathogen invasion antigen exposure Y Y Y Y YY Y Y antibodies Y Y Y alert

36. AIDS Inherited or acquired immune deficiency disorder T and B cells, so also plasma cells, never form HIV infects macrophages, T H cells and antigen presenting cells Immune response starts but then fails HIV may decrease but then the immune system fails

37. http://bcs.whfreeman.com/thelifewire/conten t/chp18/1802004.html http://bcs.whfreeman.com/thelifewire/conten t/chp18/1802004.html