PowerPoint presentation of immunology and serology

Presentation of immunology and serology

1. Immunity: An Overview

2. Introduction to Immunology…… Immunis =“exempt;” •To get rid of foreign particles in our body Our Immune system involves the inter play between our Non-specific and our Specific Immune responses.

3. Immune Response We have specific and a non-specific response sytems Non-Specific = barriers, like skin and mucus, HCl in the stomach, and phagocytosis. Specific = Immune system and antibodies

4. Role of Histamine Histamine is a hormone which is released at a damaged site Inflammation causes dilation of blood vessels More phagocytes are delivered to the damaged area.

5. Our 1 st Line of Defense... The Integumentary System… Skin Mucous membranes Mucous provides a physical barrier preventing microbial access

6. The Invaders . . . Bacteria Viruses parasites such as fungi, protista, & worms

7. Other mechanisms of Defense... Physiological variables pH of our environment temperature of our environment chemical defenses nitric oxide, enzymes, proteins, complement AND the IMMUNE SYSTEM

8. Immune System : 2 branches The Innate Immune system = a general response to anything other than recognized “self cells” The Adaptive Immune System = a specific counter-assault against a “known foreign” invader [previously recognized]

9. Major Concepts - What Happens during an infection ? How can immune cells distinguish foreign invaders from our own cells ?

10. What Happens during an infection? Innate Immunity - the troops are called to battle… injury & infection macrophages slip between cells [extravasation] to arrive cytokine chemicals attract other “troops” [chemotaxis] histamine chemicals dilate blood vessels for easier access to injury [vasodilation]

11. What are macrophages ? Phagocytic cells - able to ingest small foreign invaders neutrophils monocyte they release cytokines that enhance the immune response

12. Mast cells /basophils release histamine that dilates blood vessels causes redness [erythrema], swelling [edema], and heat [fever

13. End of part 1 Welcome to the wonders of Immunity

14. Summary: Macrophages are able to launch the first strike… more help is needed to overcome rapidly reproducing invaders… Help from the ADAPTIVE IMMUNE System results in a coordinated successful defense ! Major players . . . the B lymphocytes

15. How can antibodies distinguish our self from foreign invaders? Adaptive/Acquired Immune System - function There are 2 types of lymphocytes: T lymphocytes [ T - Helper cells ] - help signal immune cells into action B lymphocytes [ B cells ] - make special proteins called antibodies  

16. How can antibodies distinguish our self from foreign invaders? Adaptive Immune System - origin There are 2 types of lymphocytes T lymphocytes – [ T - Helper cells ] B lymphocyte begin in the red bone marrow

17. & migrate to the thymus gland ... Identification tag is a protein called Major Histocompatability Complex [MHC]

18. & in the thymus gland . . . All diversely varying MHC lymphocytes will wait for a call to action . . . These Lymphocytes will mature into T-Helper cells They function to stimulate B cells to activate their attack against the invaders

19. Adaptive Immune System The 2nd type of lymphocyte is: B lymphocytes [ B cells] - start in the bone marrow and circulate through the body they are called into action when stimulated by a foreign antigen. . . [ usually a protein from the invader]

20. When an invader attacks. . . An antigen is phagocytozed by the B cell is broken into non-infective pieces & attached to the cell’s MHC when processed through the cell’s machinery MHC-antigen complex is placed on the cell membrane surface where it is recognized by the T Helper cell

21. When help arrives . . . The T-helper cell receptor “docks” with the B cell’s MHComplex B cells proliferate . . .

22. cells differentiate into . . . Antibody producing cells [attack mode] Memory cells [remembers & future protection]

23. The RESULT . . . The Antibody producing B cells mounts a successful attack against the invader the memory B cells save the “recognition ID” for many years in preparation for future invasion

24. The RESULT . . . The Antibody producing B cells mounts a successful attack against the invader the memory B cells save the “recognition ID” for many years in preparation for future invasion

25. Cells of the Immune System White Blood Cells Phagocytes - Neutrophils - Macrophages Lymphocytes Phagocytes = Produced throughout life by the bone marrow. Scavengers – remove dead cells and microorganisms.

26. Neutrophils 60% of WBCs ‘Patrol tissues’ as they squeeze out of the capillaries. Large numbers are released during infections Short lived – die after digesting bacteria Dead neutrophils make up a large proportion of puss.

27. Macrophages Larger than neutrophils. Found in the organs, not the blood. Made in bone marrow as monocytes , called macrophages once they reach organs. Long lived Initiate immune responses as they display antigens from the pathogens to the lymphocytes .

28. Macrophages

29. Phagocytosis

30. Phagocytosis If cells are under attack they release histamine. Histamine plus chemicals from pathogens mean neutrophils are attracted to the site of attack. Pathogens are attached to antibodies and neutrophils have antibody receptors . Endocytosis of neutrophil membrane 🡪 phagocytic vacuole. Lysosomes attach to phagocytic vacuole 🡪 pathogen digested by proteases

31. Lymphocytes Produce antibodies B-cells mature in bone marrow then concentrate in lymph nodes and spleen T-cells mature in thymus B and T cells mature then circulate in the blood and lymph Circulation ensures they come into contact with pathogens and each other

32. B -Lymphocytes There are 10 million different B-lymphocytes, each of which make a different antibody. The huge variety is caused by genes coding There are a small group of clones of each type of B-lymphocyte

33. B -Lymphocytes At the clone stage antibodies do not leave the B-cells. The antibodies are embedded in the plasma membrane of the cell and are called antibody receptors. When the receptors in the membrane recognises an antigen on the surface of the pathogen the B-cell divides rapidly. The antigens are presented to the B-cells by macrophages

34. B -Lymphocytes

35. B -Lymphocytes Some activated B cells 🡪 PLASMA CELLS these produce lots of antibodies, < 1000/sec The antibodies travel to the blood, lymph, lining of gut and lungs. The number of plasma cells goes down after a few weeks Antibodies stay in the blood longer but eventually their numbers go down too.

36. B -Lymphocytes Some activated B cells 🡪 MEMORY CELLS . Memory cells divide rapidly as soon as the antigen is reintroduced. There are many more memory cells than there were clone cells. When the pathogen/infection infects again it is destroyed before any symptoms show.

37. B Memory Cells Stay in our tissues for many years. They carry out mitosis immediately upon contact with the complementary antigen A very quick, secondary response We do not become ill The same process with T memory cells

38. T-Lymphocytes Mature T-cells have T cell receptors which have a very similar structure to antibodies and are specific to 1 antigen. They are activated when the receptor comes into contact with the Ag with another host cell (e.g. on a macrophage membrane or an invaded body cell

39. T-Lymphocytes After activation the cell divides to form: T-helper cells – secrete CYTOKINES 🡪 help B cells divide 🡪 stimulate macrophages Cytotoxic T cells (killer T cells) 🡪 Kill body cells displaying antigen Memory T cells 🡪 remain in body

40. How T cells protect us They kill infected cells by producing a protein which destroys the cell membrane They stimulate Phagocytes They stimulate B cells to divide They form T memory cells

41. Enjoy God’s protection!!!