18. Kuby's Immunology Online (www)
Induction of Immune ResponsesInduction 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).
19. Cells of the Immune System. In: Encyclopedia of Life Sciences (www)
20. Functions of antibodiesFunctions 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}
22. Antibody ResponsesAntibody 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)
26. 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-cell Dependence of Antibody ResponseT-cell Dependence of Antibody Response
30. Roy, 2003 (www)
Endogenous and Exogenous Antigen Presenting PathwaysEndogenous and Exogenous Antigen Presenting Pathways
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. Immune System. In: Encyclopedia of Life Sciences (www)
Endogenous and Exogenous Antigen Presenting PathwaysEndogenous and Exogenous Antigen Presenting Pathways
40. MHC I - Mediated Immune ResponseMHC I - Mediated Immune Response
Evasion by CMVEvasion by CMV
New Science Primers: Immunity (www)
41. Immune Evasion ExamplesImmune 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
