Maturation involves signal-regulated adjustments in cells/immune cells/thymocytic cells that lead to cellular specialization.

stem → progenitor → precursor → adult → mature

B thymocyte → B lymphocyteplasma cells or memory B cells
T thymocyte → T lymphocyteTcCTL, some CTLCIK
______________-________helper T cells
______________-________regulatory T cells
______________-________natural killer T cells

Dendritic cells (DC) are the most potent antigen presenting cells of the immune system. A variety of factors operate in antigen recognition and processing by immature (precursor) dendritic cells and in the maturation of immature cells. Toll-like receptors on the surfaces of precurson dendritic cells recognize microbial components and induce the differentiation of dendritic cell precursors. GM-CSF and IL-4 stimulate the maturation of monocytopoietic pDC1, while IL-3 stimulates the differentiation of pDC2. The stimulatory capacity (maturation) of DCs plus their the expression of CD40, CD54, CD58, CD80, CD83, CD86 and MHC class II molecules is enhanced by eicosanoid-fatty acid-prostaglandins: PGE2 > PGE1 > PGF2α > PGI2 (prostacyclin). PG effects on the maturation of DC and enhanced T cell proliferation are mimicked by db-cAMP and forskolin, indicating that maturation effects are due to elevated cAMP levels. Maturation of DCs is accompanied by secretion of higher levels of proinflammatory cytokines IL-1β, IL-6, TNF-α, and IL-12, enhancing DC capacity to induce a Th1 immune response.

Affinity maturation is a process of affinity-selected differentiation of activated B cells. Repeated exposures to the same antigen provokes greater antibody ligating affinity in the antibody secreted by successive generations of plasma cells. Somatic mutations mediate the maturation of T-dependent humoral immune responses. Clones of B cell clones that express antibodies with progressively increased affinity are selected by antigen-signaling from somatic variants of germ-line-encoded genes. However, such antigen selection cannot explain the emergence of B cell clones secreting rather low-affinity antibodies and the shift to alternative germ-line V region gene combinations occurring during secondary and tertiary responses. Idiotypic suppression may favor this clonal shift. Idiotypic recognition in the syngeneic host that is highly restricted to private idiotopes of each clone sequentially activated during immune maturation could explain the phenomenon.[pm] Џ B cell maturation - animation Џ

Tables  Cell signaling  Complement Receptors  Cytokines  Eicosanoid Actions  Fc receptors  Immunoglobulins  Interferons  Receptor Tyrosine Kinases (RTKs)  Receptor Signal Transduction  Second Messengers  Scavenger Receptors  Toll-like Receptors


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