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, B LYMPHOCYTE T LYMPHOCYTE
neutrophils
NK CELLS Phagocytosed Intracellular
microbes microbes
INTERFERON, INTERLEUKIN,
CHEMOKINE, TNF Th Tc
COMPLEMENT SYSTEM
INITIAL CONTROL NEUTRALISATION MACROPHAGE CYTOTOXICITY
OF INFECTION ACTIVATION
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)
(www)
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)
(www)