1. Immunology in a Nutshell
M. Tevfik DORAK

2. Immune System INNATE IMMUNITY ADAPTIVE IMMUNITY PHYSICAL BARRIERS
CHEMICAL PROTECTION
HUMORAL IMMUNITY
CELLULAR IMMUNITY
Pathogen associated molecular patterns
Extracellular microbes
PHAGOCYTES
Monocyte/macrophage, neutrophils
B LYMPHOCYTE
T LYMPHOCYTE
NK CELLS
Phagocytosed microbes
Intracellular microbes
INTERFERON, INTERLEUKIN, CHEMOKINE, TNF Th Tc
COMPLEMENT SYSTEM
NEUTRALISATION
MACROPHAGE ACTIVATION
CYTOTOXICITY
INITIAL CONTROL OF INFECTION

3. Innate & Adaptive Immunity Timeline
Cambridge University Immunology Lectures (www)

4. Bone Marrow Derived Cells
Hoffbrand (www)

5. Normal White Blood Cells
Hoffbrand (www)

6. Normal White Blood Cells
Hoffbrand (www)

7. Hoffbrand (www)

8. Components of the Immune System
Immune System. In: Encyclopedia of Life Sciences (www)

9. Components of the Immune System
Immune System. In: Encyclopedia of Life Sciences (www)

10. Manson's Tropical Disease: Genetics (www)

11. Innate Immunity: Toll-Like Receptors
Wagner, 2004 (www)

12. Innate Immunity: Toll-Like Receptors
New Science Primers: Immunity (www)

13. Reticuloendothelial System
Hoffbrand (www)

14. Acute Phase Reaction
Immune System. In: Encyclopedia of Life Sciences (www)

15. Complement Activation
Cambridge University Immunology Lectures (www)

16. Immune System. In: Encyclopedia of Life Sciences (www)

17. Complement Pathway
Souhami & Mouxham (www)

18. Induction of Immune Responses
Activation and proliferation of TH cells. (a) is required for generation of humoral response (b) and cell-mediated response to altered self-cells (c).
Kuby's Immunology Online (www)

19. Cells of the Immune System. In: Encyclopedia of Life Sciences (www)

20. Functions of antibodies
Neutralization
Agglutination (antigen cross-linking)
Complement activation (classical pathway)
Antibody-dependent cell-mediated cytotoxicity (ADCC)
{Fc receptors - NK cells}
Opsonization
{Fc receptors - phagocytes}
Degranulation of inflammatory cells
{Fc receptors - macrophages, basophils, eosinophils}

21. Antibody Responses
Souhami & Mouxham (www)

22. Antibody Responses
Once activated by direct interaction with antigens and with some help from TH cells, some B-cell become IgM secreting plasma cells. Some migrate to the B cell rich areas of lymph nodes and form germinal centres. Here B cells proliferate and give rise to progeny with high affinity for antigen through a process called affinity maturation. The products of germinal centres become IgG, A etc, plasma cells and memory B cells.
Cambridge University Immunology Lectures (www)

23. Antibodies
Souhami & Mouxham (www)

24. Antibodies
Hoffbrand (www)

26. T-cell Dependence of Antibody Response
Protein antigens do not induce antibody responses in the absence of T lymphocytes, they are T-dependent. The antibodies to these antigens go through affinity maturation resulting in development of strong memory responses.
Non-protein antigens, polysaccharides and lipids for example, can give antibody responses without T cells (T-independent). T independent antigens are usually polymeric and it is believed that they cross link membrane Ig on B cells sufficiently well to activate them without co-operation from T cells. The antibodies to these antigen are invariably IgM and do not demonstrate affinity maturation.

27. T Helper Cells
Hoffbrand (www)

28. B and T-cell Interactions
Dube, 2002 (www)
eBiosciences Poster (www)

29. (www)

30. Endogenous and Exogenous Antigen Presenting Pathways
Roy, 2003 (www)

31. Figure 1. Professional antigen-presenting cells process intracellular and extracellular pathogens differently. In the endogenous pathway, proteins from intracellular pathogens, such as viruses, are degraded by the proteasome and the resulting peptides are shuttled into the endoplasmic reticulum (ER) by TAP proteins. These peptides are loaded onto MHC class I molecules and the complex is delivered to the cell surface, where it stimulates cytotoxic T lymphocytes (CTLs) that kill the infected cells. In contrast, extracellular pathogens are engulfed by phagosomes (exogenous pathway). Inside the phagosome, the pathogen-derived peptides are loaded directly onto MHC class II molecules, which activate helper T cells that stimulate the production of antibodies. But some peptides from extracellular antigens can also be 'presented' on MHC class I molecules. How this cross-presentation occurs has now been explained: it seems that by fusing with the ER, the phagosome gains the machinery necessary to load peptides onto MHC class I molecules. Roy, 2003 (www)

32. Endogenous and Exogenous Antigen Presenting Pathways
Immune System. In: Encyclopedia of Life Sciences (www)

33. Thomas & Arend: Antigen Presenting Cells (www)

34. Thomas & Arend: Antigen Presenting Cells (www)

35. MHC II - Mediated Immune Response
Hoffbrand (www)

38. Nakachi, 2004 (www)

39. Nakachi, 2004 (www)

40. MHC I - Mediated Immune Response Evasion by CMV
New Science Primers: Immunity (www)

41. Immune Evasion Examples
Mycobacteria : Inhibits phagolysosome fusion so that it survives within the phagosome
Herpes simplex virus : Interferes with TAP transporter (inhibits antigen presentation)
Cytomegalovirus : Inhibits proteasome activity and removal of MHC I from ER
Epstein-Barr virus : Inhibits proteasome activity; produces IL-10 to inhibit
macrophage activation
Pox virus : Produces soluble cytokine receptors to inhibit activation of
effector cells

42. Cytokines
Souhami & Mouxham (www)

43. Pleiotropic Effects of Interleukin-1
Hoffbrand (www)

44. Pleiotropic Effects of Interleukin-6
Hoffbrand (www)

45. (www)