Immunology in a Nutshell M. Tevfik DORAK http://www.dorak.info

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

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

Bone Marrow Derived Cells Hoffbrand (www)

Normal White Blood Cells Hoffbrand (www)

Normal White Blood Cells Hoffbrand (www)

Hoffbrand (www)

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

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

Manson's Tropical Disease: Genetics (www)

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

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

Reticuloendothelial System Hoffbrand (www)

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

Complement Activation Cambridge University Immunology Lectures (www)

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

Complement Pathway Souhami & Mouxham (www)

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)

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

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}

Antibody Responses Souhami & Mouxham (www)

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)

Antibodies Souhami & Mouxham (www)

Antibodies Hoffbrand (www)

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.

T Helper Cells Hoffbrand (www)

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

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

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)

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

Thomas & Arend: Antigen Presenting Cells (www)

Thomas & Arend: Antigen Presenting Cells (www)

MHC II - Mediated Immune Response Hoffbrand (www)

Nakachi, 2004 (www)

Nakachi, 2004 (www)

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

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

Cytokines Souhami & Mouxham (www)

Pleiotropic Effects of Interleukin-1 Hoffbrand (www)

Pleiotropic Effects of Interleukin-6 Hoffbrand (www)

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