B cell proliferation

Solid organ transplant recipients have a blunted immune response to vaccines because the immunosuppressive regimens used to prevent organ rejection inhibit both T- and B-cell proliferation. Many of these patients will also have secondary hypogammaglobulinemia post-transplantation. Prior to transplant, children should complete primary immunization schedules if possible accelerated schedules may be used. Adults should have all vaccinations updated prior to transplantation.16... 

Harnett, W. and Harnett, M.M. (1993) Inhibition of murine B cell proliferation and down-regulation of protein kinase C levels by a phosphorylcholine-containing filarial excretory-secretory product. Journal of Immunology 151, 4829-4837. 

Brunswick, M., Finkelman, F.D., Higher P.F., Inman, J.K., Dintzis, H.M., and Mond, J.J. (1988) Picogram quantities of anti-Ig antibodies coupled to dextran induce B cell proliferation. /. Immunol. 140, 3364-3372. 

Lymphocyte-activating factor enhances activation of T and B cells, NK cells, and macrophages T-cell growth factor stimulates T-cell growth and effector differentiation stimulates B-cell proliferation/differentiation Mast-cell growth factor stimulates... 

FUNCTION MEDIATES B-CELL PROLIFERATION IN THE ABSENCE OF COSTIMULUS AS WELL AS IGE PRODUCTION IN THE PRESENCE OF IL-4. INVOLVED IN IMMUNOGLOBULIN CLASS SWITCHING. 

B cells are produced by the bone marrow. In response to activation of CD4+ T helper cells (see below), B cells proliferate and produce antibodies. (The term CD stands for cluster of differentiation. They are proteins coating cell surfaces. Altogether, there are more than 160 different types of CDs.) The antibodies produced by B cells circulate in the bloodstream and bind to antigens. Once bound, other cells are in turn activated to destroy the antigens. 

Acetaldehyde, benzene, butyraldehyde, iso-prene, styrene, and toluene in mouse lymphocytes cell culture for 3 hours produced no effect on either viability or proliferation. Lormaldehyde, catechol, acrylonitrile, propionaldehyde, and hydroquinone significantly inhibited T-lymphocyte and B-lymphocyte proliferation, inhibitory concentration (IC )jo 1.19 x 10" M to 8.20 x 10" M. Acrolein and crotonaldehyde inhibited T-cell and B-cell proliferation and acted on viability with ICjp 2.06 x 10 M to 4.26 X 10" M. Mixtures of acrolein, formaldehyde, and propionaldehyde or crotonaldehyde interactive effects at 0.5 and 1 x ICjo were observed " . 

Interleukin-1 QL-l) T cell activation, B cell proliferation and differentiation... 

Costinean S, Zanesi N, Pekarsky Y et al. Pre-B cell proliferation and lymphoblastic leukemia/high-grade lymphoma in E(mu)-miR155 transgenic mice. Proc Natl Acad Sci USA 2006 103 7024-7029. Volinia S, Calin GA, Liu CG et al. A microRNA expression signature of human solid tumors defines cancer gene targets. Proc Natl Acad Sci USA 2006 103 2257-2261. 

After recognizing antigens through membrane-bound antibodies, there is B cell proliferation and differentiation for about 4-5 days. This results in the production of plasma and memory cells. One of the five classes of antibodies are produced and secreted by plasma cells that do not possess membrane-bound antibodies. Plasma cells survive for about 1-2 weeks. 

Indomethacin, introduced in 1963, is an indole derivative (Figure 36-1). It is a potent nonselective COX inhibitor and may also inhibit phospholipase A and C, reduce neutrophil migration, and decrease T cell and B cell proliferation. Probenecid prolongs indomethacin s half-life by inhibiting both renal and biliary clearance. 

Sulfasalazine is metabolized to sulfapyridine and 5-aminosalicylic acid, and it is thought that the sulfapyridine is probably the active moiety when treating rheumatoid arthritis (unlike inflammatory bowel disease see Chapter 63 Drugs Used in the Treatment of Gastrointestinal Diseases). Some authorities believe that the parent compound, sulfasalazine, also has an effect. In treated arthritis patients, IgA and IgM rheumatoid factor production are decreased. Suppression of T cell responses to concanavalin and inhibition of in vitro B cell proliferation have also been documented. It is not clear how these findings relate to the clinical efficacy of sulfasalazine in rheumatoid arthritis. 

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