3. First Line of Defense  Skin & mucous membranes Physical barrier Chemical barrier ○ Lower pH ○ “Flushing” of invades (tears, sweat, mucus) ○ Antimicrobial proteins (lysozymes) Digest cell walls

4. Second Line of Defense  Non-specific  Phagocytic leukocytes (WBC) Neutrophils (60-70%) ○ Attracted to chemical signals from damaged cells (chemotaxis) ○ Engulf & destroy microbes

5. Second Line of Defense Monocytes (5%) ○ Develop into long-lasting microphages Attach to polysaccharides on microbe’s surface ○ Some migrate, some are permanent in lungs, liver, kidneys, brain, connective tissues, lymph nodes, & spleen

7. Second Line of Defense Eosinophils (1.5%) ○ Defend against larger parasitic invaders Natural killer cells (NK) ○ Destroy virus-infected body cells

8. Second Line of Defense  The Inflammatory Response Precapillary arterioles dilate Postcapillary venules constrict ○ Inc. blood supply (redness & heat) ○ Pushes fluid out (edema)

9. Second Line of Defense Initiated by chemical signals ○ Histamine Produced by basophils (type of WBC) and mast cells in connective tissue Increase dilation ○ Prostaglandins Promote blood flow to injury site Both inc. addition of clotting factors to the area for healing

10. Second Line of Defense Phagocytic cells attracted to area by chemokines (secreted by blood vessel endothelial cells & monocytes) Pyrogens ○ Released by leukocytes ○ Raise body temp ○ Inhibit growth & facilitate phagocytosis

11. Third Line of Defense  Specific Immunity Lymphocytes ○ B cells & T cells ○ In spleen, lymph nodes, & lymphatic tissues ○ Detect specific antigens Foreign molecules that elicit specific response ○ Activate & produce certain antibodies ○ Have membrane antigen receptors

12. Third Line of Defense ○ During early development, B cell or T cell develops receptors for any type of antigen (before contact) ○ When contact with antigen, lymphocyte divides, differentiates, forming two clones Effector cells (secrete antibody) Memory cells (long-living; have receptors for antigen)

14. Third Line of Defense  First contact – primary immune response  Second contact – secondary I.R. Quicker (due to memory) Larger scale

15. Lymphocyte Development  From pluripotent stem cells Fetal bone marrow & liver If then move to thymus  T cell If stays in bone marrow  B cell  Key: self vs non-self If not, apoptosis

16. Major Histocompatibility Complex (MHC)  Cell surface glycoproteins  Mark body cells as “self”  Class I: on all nucleated cells  Class II: specialized (macrophages & B cells) Known as Antigen Presenting Complex (APC)

17. Major Histocompatibility Complex (MHC)  Very polymorphic Makes almost all people unique  When infection, MHC presents antigen to T cell to alert them (antigen presentation)  Class I present to cytotoxic T cells (T C )  Class II present to helper T cells (T H )

20. Immune Response  Humoral Immunity B cell activation Results from production of antibodies that move in plasma & lymph Defend free invaders in body fluid

22. Immune Response  Cell-mediated immunity T cell activation When cytotoxic T cell activated by Class I MHC, becomes active killer ○ Kills target cell with perforin Protein that forms pores in target cell membrane

28. Invertebrate Immune System  Non specific defense (mostly)  Self vs nonself  Cytokines present  Some produce antibody-like proteins Insects: hemolin is an immunoglobulin  No memory cells (mostly)

29. Plant Immune System  Plant defenses include molecular recognition systems with systemic responses  Infection triggers chemical responses Destroy infected and adjacent cells, thus localizing the effects.

30. Immunity Applications  Active immunity Achieved by exposure & recovery or vaccination  Passive immunity Receiving antibodies  Blood Compatibility Based on surface antigen of RBC

32. Immunity Applications  Rh factor RBC antigen (IgG) Mom Rh-, fetus Rh+ ○ Mother may have a T-dependent humoral response Affects subsequent pregnancies -Memory cells produce IgG

33. Immunity Applications  Tissues & Organs MHC can cause rejection  Allergies Exaggerated responses to envi. antigens Tend to involve IgE & mast cells Release of histamine Can result in abrupt dilation of blood vessls, lowering bp (anaphylactic shock)

35. Immunity Applications  Autoimmune Diseases Turns against itself Lupus, MS, diabetes, rheumatoid arthritis

36. Immunity Applications  SCID Both humoral & cell-mediated problems Hodgkin’s disease ○ Damages lymphatic system

37. Immunity Applications  AIDS Caused by HIV HIV-1 (more virulent strain) & HIV-2 Both infect cells that have surface CD4 molecules Can also infect helper T cells, B lymphocytes, & brain cells

38. Immunity Applications Entry of virus requires CD4 & a coreceptor protein ○ Fusin (CXCR4), found on helper T cells ○ CCR5, found on macrophages Integrates into genome Body makes HIV antibodies intially

39. Immunity Applications Over time, viral load increases Helper T cells become infected & die Use DNA-synthesis inhibitors, reverse transcriptase inhibitors, & protease inhibitors to combat