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Memory B-cells

Muehlinghaus G, Cigliano L, Huehn S, et al. Regulation of CXCR3 and CXCR4 expression during terminal differentiation of memory B cells into plasma cells. Blood 2005 105 3965-3971. [Pg.117]

Somatic hypermutation Mutations occurring in the variable region genes of the light and heavy chains during the formation of memory B cells. Those B cells whose affinity is increased by such mutations are positively selected by interaction with antigen, and this leads to an increase in the average affinity of the antibodies produced. [Pg.253]

Vajdy, M. (2006). Generation and maintenance of mucosal memory B cell responses Curr. Med. Chem. 13(25) 3023-3037. [Pg.174]

The IgG described above is the major antibody in secondary immune responses, which are initiated by memory B cells. As part of the organism s ongoing immunity to antigens already encountered and dealt with, IgG is the most abundant immunoglobulin in the blood. When IgG binds to an invading bacterium or virus, it... [Pg.179]

MacLennan, I.C.M. Gray, D. (1986). Antigen-driven selection of virgin and memory B cells. Immunol. Rev. 91,61-85. [Pg.81]

If an injection of Rh0(D) antibody is administered to the mother within 24-72 hours after the birth of an Rh-positive baby, the mother s own antibody response to the foreign Rh0(D)-positive cells is suppressed because the baby s red cells are cleared from circulation before the mother can generate a B cell response against Rh0(D). Therefore, she has no memory B cells that can activate upon subsequent pregnancies with an Rh0(D)-positive fetus. [Pg.1347]

The final stage of B cell differentiation where the BCR repertoire is shaped is the germinal centre (GC) reaction. In the T cell dependent GC reaction, the BCR is adapted for its cognate antigen by somatic hypermutation (SMH) and class switch recombination (CSR), both of which are driven by activation induced cytidine deaminase (AID). Since AID induces targeted point mutations in the CDRs of the Ig HCs and Ig LCs, this can dramatically alter the BCR affinity or even its specificity. As AID activity may also result in the formation of an autoreactive BCR, a stringent counterselection of such self-reactive B cells is required. By analysis in human of the BCR repertoire of post-GC IgG+ memory B cells, it was demonstrated that indeed new auto-reactive B cells develop by SHM whereas 20% of naive B cells is self-reactive, up to 40% of the IgG+ memory B cells expressed a true de novo created self-reactive BCR. Apparently, lack of T cell help prevents activation of these self-... [Pg.164]

As described above, peptide epitopes bound to MHC class I or II molecules are able to stimulate CD8+ and CD4+ T cells, respectively. Both CD4+ T-helper cells and CD8+ CTLs are critical to protective immunity and to vaccine efficacy. CD4+ T-helper cells play an important role in the development of memory B-cell (antibody) and memory CTL (cytotoxic T-cell) responses. CD4+ T-helper cells are also active against pathogens on their own. Therefore, CD4+ T-helper cells have been called the conductors of the immune system orchestra (14). CD8+ CTLs are able to directly kill infected target cells and thus are critical in the containment of... [Pg.121]

Klein U, Kiippers R, Rajewsky K, Evidence for a large compartment of IgM-expressing memory B cells in humans, Blood, 89 1288-1298, 1997. [Pg.465]

Memory B-cells respond to subsequent infection by that antigen... [Pg.236]

Ettinger R, Sims GP, Fairhurst AM, Robbins R, Da Silva YS, Spolski R, Leonard WJ, Lipsky PE (2005) 11-21 induces differentiation of human naive and memory B cells into antibody-secreting plasma cells. J Immunol 175 7867-7879. [Pg.150]


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See also in sourсe #XX -- [ Pg.493 , Pg.493 ]




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B cells

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