Immunity [M.Tevfik DORAK]

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Immunology in a Nutshell
M. Tevfik DORAK http//www.dorak.info
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Immune System
INNATE IMMUNITY
ADAPTIVE IMMUNITY
PHYSICAL BARRIERS
HUMORAL IMMUNITY
CELLULAR IMMUNITY
CHEMICAL PROTECTION
Pathogen associated molecular patterns
Extracellular microbes
PHAGOCYTES Monocyte/macrophage, neutrophils
B LYMPHOCYTE
T LYMPHOCYTE
Phagocytosed microbes
Intracellular microbes
NK CELLS
INTERFERON, INTERLEUKIN, CHEMOKINE, TNF
Th
Tc
COMPLEMENT SYSTEM
NEUTRALISATION
MACROPHAGE ACTIVATION
CYTOTOXICITY
INITIAL CONTROL OF INFECTION
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Innate Adaptive Immunity Timeline
Cambridge University Immunology Lectures (www)
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Bone Marrow Derived Cells
Hoffbrand (www)
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Normal White Blood Cells
Hoffbrand (www)
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Normal White Blood Cells
Hoffbrand (www)
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Hoffbrand (www)
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Components of the Immune System
Immune System. In Encyclopedia of Life Sciences
(www)
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Components of the Immune System
Immune System. In Encyclopedia of Life Sciences
(www)
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Manson's Tropical Disease Genetics (www)
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Innate Immunity Toll-Like Receptors
Wagner, 2004 (www)
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Innate Immunity Toll-Like Receptors
New Science Primers Immunity (www)
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Reticuloendothelial System
Hoffbrand (www)
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Acute Phase Reaction
Immune System. In Encyclopedia of Life Sciences
(www)
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Complement Activation
Cambridge University Immunology Lectures (www)
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Immune System. In Encyclopedia of Life Sciences
(www)
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Complement Pathway
Souhami Mouxham (www)
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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)
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Cells of the Immune System. In Encyclopedia of
Life Sciences (www)
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Functions of antibodies Neutralization Agglutin
ation (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
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Antibody Responses
Souhami Mouxham (www)
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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)
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Antibodies
Souhami Mouxham (www)
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Antibodies
Hoffbrand (www)
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(No Transcript)
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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.
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T Helper Cells
Hoffbrand (www)
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B and T-cell Interactions
Dube, 2002 (www) eBiosciences Poster (www)
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(www)
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Endogenous and Exogenous Antigen Presenting
Pathways
Roy, 2003 (www)
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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)
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Endogenous and Exogenous Antigen Presenting
Pathways
Immune System. In Encyclopedia of Life Sciences
(www)
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Thomas Arend Antigen Presenting Cells (www)
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Thomas Arend Antigen Presenting Cells (www)
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MHC II - Mediated Immune Response
Hoffbrand (www)
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(No Transcript)
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(No Transcript)
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Nakachi, 2004 (www)
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Nakachi, 2004 (www)
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MHC I - Mediated Immune Response Evasion by CMV
New Science Primers Immunity (www)
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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
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Cytokines
Souhami Mouxham (www)
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Pleiotropic Effects of Interleukin-1
Hoffbrand (www)
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Pleiotropic Effects of Interleukin-6
Hoffbrand (www)
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(www)