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Class switch induction

IL-4 TH2 cells, mast cells, NK cells B cells, T cells, mast cells, macrophages Proliferation, isotype switching, induction of MHC class II expression... [Pg.47]

Figure 32.9. Schematic representation of Type I hypersensitivity. Induction Resident respiratory tract dendritic cells (DC) take and process antigen, mature, migrate to the draining lymph nodes, and present antigen to T lymphocytes. Activated T-lymphocytes, in turn, activate B-cell differentiation into antibody-producing plasma cells. IL-4 promotes Ig isotype class switching from IgM to IgE and promotes mast cell development. IgE is associated with mast cells. Elicitation Allergen crosslinks the mast-cell-bound IgE, thereby causing the release of preformed mediators and cytokines. (See Table 32.7.) Inflammation and bronchoconstriction occur. Figure 32.9. Schematic representation of Type I hypersensitivity. Induction Resident respiratory tract dendritic cells (DC) take and process antigen, mature, migrate to the draining lymph nodes, and present antigen to T lymphocytes. Activated T-lymphocytes, in turn, activate B-cell differentiation into antibody-producing plasma cells. IL-4 promotes Ig isotype class switching from IgM to IgE and promotes mast cell development. IgE is associated with mast cells. Elicitation Allergen crosslinks the mast-cell-bound IgE, thereby causing the release of preformed mediators and cytokines. (See Table 32.7.) Inflammation and bronchoconstriction occur.
Mandler, R., Finkelman, F.D., Levine, A.D. and Snapper, C.M. (1993). IL-4 induction of IgE class switching by lipopolysaccharide-artivated murine B cells occurs predominantly through sequential switching. J. Immunol. 150, 407-418. [Pg.50]

Lester et al. [56] showed that TSST-1 at 1 pg/ml inhibited IL-4-stimulated synthesis of IgE, but not of IgG, in PBMCs from AD patients and normal donors. Inhibition of IL-4-induced IgE production was associated with the induction of IFN-y secretion by TSST-1. This inhibitory effect was blocked by a neutralizing antibody against IFN-y (normal PBMC) or IFN-a (AD PBMC). (In normal blood, IFN-y exceeds IFN-a concentrations, whereas in AD blood, production of IFN-y by T cells is inhibited, but the production of IFN-a by monocytes is increased.) This provided the first clue that TSST-1 (at 1 pg/ml) might inhibit class switching to IgE by enhancing the synthesis of IFN-y and IFN-a. [Pg.117]

Due to experimental difficulties, little is known about the initial phase of class switching. Specific inductive stimuli for switching have not even been hypothesized for mammalian cells except for the isotype determination by IL-4. [Pg.140]

The molecular analysis of recombinant switch regions also sheds light on switch induction and isotype commitment. Such studies reveal that, upon activation, class switching is induced in some cells but not others. Otherwise, recombinations on the excluded IgH allele would have been found in late IgM expressing cells this... [Pg.143]

Fig. 3. Programmed class switch recombination. Upon activation the B cell starts to secrete IgM, proliferate and perform class switch recombination. In early stages recombinations within and probably other S regions are found (not shown). In later rounds of replications recombinations between switch regions accompany the phenotypic switch. These recombinations occur on both, active and inactive, IgH loci of a cell. The active locus is not necessarily rearranged first. Frequently both IgH loci show recombination between the same switch regions, indicating a pr°8ramm ng inductive event. Fig. 3. Programmed class switch recombination. Upon activation the B cell starts to secrete IgM, proliferate and perform class switch recombination. In early stages recombinations within and probably other S regions are found (not shown). In later rounds of replications recombinations between switch regions accompany the phenotypic switch. These recombinations occur on both, active and inactive, IgH loci of a cell. The active locus is not necessarily rearranged first. Frequently both IgH loci show recombination between the same switch regions, indicating a pr°8ramm ng inductive event.
Another class of devices used to control the voltage is operated using powered electronic switches to continuously adjust the capacitance and/or inductance in a substation to keep the voltage at precisely the voltage desired. These devices are relatively new in deployment, having been developed with the advent of inexpensive and robust power semiconductor components. These devices are part of a group broadly known as FACTS (Flexible AC Transmission System) devices and include static var compensators, static synchronous compensators, and dynamic voltage restorers. [Pg.432]

Thirdly, we find the optimal inductance L2 for the implanted coil using (76). With the assumption that the primary Class E power amplifier has (2i 50(switch power loss is included), the optimal inductance L2 is calculated to be 1.91/u.// and achieved by 19 turns with 12 strands. The power efficiency n] is computed to be 28% using (78). [Pg.298]

Substantial evidence has supported the role of IL-4 and IL-13 in the induction of IgE synthesis (194). Interleukin-4 and IL-13 are the only cytokines known that can induce IgE synthesis in vitro using the recombinant proteins (186,195). The role of IL-4 was initially identified in vitro, T-cell-derived IL-4 was able to induce IgE production by lipopolysaccharide (LPS)-stimulated murine B cells (196), and anti-IL-4/IL-4 receptor (IL-4R) antibodies inhibited IgE responses in experimental animals (197,198). The role of IL-4 in human IgE isotype switch in B cells from IgM to IgE has been established using normal unfractionated peripheral blood mononuclear cells (PBMCs) (199) and single B cells stimulated with murine and human T-cell clones (192,200). Interleukin-4 is produced by activated Th2-type CD4+ cells and Tc2 type CD8+ cells (201), mast cells, and basophils (202). Functions attributable to IL-4 include upregulation of surface CD23, MHC class II and IL-4 receptor expression on monocytes and B cells, and increased expression of VCAM-1 on endothelial cells. [Pg.148]


See other pages where Class switch induction is mentioned: [Pg.792]    [Pg.274]    [Pg.46]    [Pg.274]    [Pg.116]    [Pg.75]    [Pg.19]    [Pg.136]    [Pg.773]    [Pg.271]    [Pg.628]    [Pg.9]    [Pg.276]    [Pg.114]    [Pg.668]    [Pg.687]    [Pg.57]    [Pg.752]    [Pg.192]    [Pg.231]    [Pg.222]    [Pg.775]    [Pg.147]    [Pg.148]   
See also in sourсe #XX -- [ Pg.139 , Pg.143 ]




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