Professional Documents
Culture Documents
immunity
Jan eromski
2012/2013
prof. Jules A.
Hoffmann
(France)
POINTS TO BE DISCUSSED
GENERAL PROPERTIES OF
CYTOKINES (CT)
Production induced by: a) microbial products in
innate immunity, b) foreign antigens in acquired
immunity, c) own metabolites
Short secretion transient and unstable activation
of transcription
Lack of stability of mRNA
Pleiotropic action on various cells, organs and
systems
ROUTES OF
CYTOTOXICITY
ANGRY
MACROPHAGE
FEATURES OF ACTIVATED
MACROPHAGES
Increased expression of MHC molecules
Increased expression of costimulators (B7-1 and B72, CD40)
Secretion of cytokines (TNF, IL-1, IL-12, IL-18,
IFN, PDGF)
Secretion of chemokines
Expression of enzymes catalysing the production of
microbicidal substances in phagolysosomes (ROI,
nitric oxide, proteolytic enzymes)
POTENTIAL MECHANISMS OF
CYTOTOXICITY OF MYELOID CELLS
Lysozyme, C3a
POTENTIAL MECHANISMS OF
CYTOTOXICITY OF MYELOID CELLS-2
Hydrolases
Contribute to or cause:
1. Hypersensitivity reactions such as
tissue damage in several infectious
diseases,
2. Some autoimmune diseases,
3. Organ transplant rejection,
4. Graft-vs-host disease.
OVERVIEW OF LYMPHOCYTE
RESPONSES
FEATURES OF NK CELLS
Granular lymphocytes, express CD16 and
CD56, but NOT CD3
Spontaneously cytotoxic to certain tumors
and virally infected cells
Found in the blood, spleen, lung, liver, GI
tract and uterine decidua
Activated by IL-2, IL-12, IL-15 or IL-18
FEATURES OF NK CELLS -2
Subsets express killer immunoglobulin-like
receptors (KIR) for class I MHC antigens.
Long ones possess ITIM (immunoreceptor
tyrosine based inhibitory motif) domain
(inhibitory), while short ones have ITAM
domain providing activatory (death) signal
Target cell lysis via perforin/granzymes
pathways and receptor induced apoptosis
Ligands
Class I HLA-C alleles
CYTOTOXICITY OF NK CELLS
EFFECTOR FUNCTIONS
OF ANTIBODIES
Neutralization of microbes (bacteria and viruses)
Inactivation of toxins
Opsonization of microbes with subsequent
phagocytosis
Antibody dependent cellular cytotoxicity (ADCC)
Activation of classical pathway of complement
(IgG, IgM)
Mast cell and basophil degranulation (IgE)
CYTOTOXICITY of COMPLEMENT
THANK YOU!