B cell activating factor

B cell activating factor B cell attracting chemokine... 

BLys B lymphocyte stimulator B-cell activating factor, BAFF... 

Fibroblast activating factor B-cell growth factor Prostaglandins... 

Although the mechanism of action of IFN-a against HCL is incompletely understood, it most likely relates to IFN-a-induced B-cell differentiation, inhibition of hairy-cell responsiveness to B-cell growth factors, or activation of antineoplastic immune cell function [83]. 

Interleukin-2 (T-cell growth factor Fig. 30-6A) is secreted by some activated T-lymphocytes. This 133-residue largely helical protein is involved in generation of cytotoxic T-cells, stimulation of interferon release, and of release of a B-cell growth factor.269 Considerable excitement has accompanied the possibility of activating lymphocytes with IL-2 produced from cloned genes in bacteria to increase their ability to kill cancer cells. However, IL-2 is toxic, and this is limiting its use. See also Chapter 31, Section C. 

This is converted to an inactive phosphorylated form by a dsRNA-dependent protein kinase205 (Fig. 31-10). The protein kinase also appears to be an interferon-induced protein206 as is the oligo(2 -5 A)-activated RNAse indicated in Fig. 31-10.207 Interferons have effects other than inducing the antiviral state. Thus, human IFN-(32 is identical to a B-cell differentiation factor.208 Both IFN-a and IFN-(3 have antigrowth activity and are currently in use for treatment of some forms of cancer as well as for viral infections.209... 

Yokota T, Otsuka K, Mosmann T, Banchereau J, et al. 1986. Isolation and characterization of a human interleukin cDNA clone, homologous to mouse B-cell stimulatory factor 1, that expresses B-cell and T-cell stimulating activities. Proc Nat Acad Sci USA. 83 5894-5898. 

Rheumatoid factors of the IgM and IgG classes have been shown to form immune complexes in serum or joint fluid either by self-association (K17, M4, M26, P13, Sll, W21) or by reaction with native IgG (C4, K17, M4, N5, Sll, W21, W22), and these appear to be the predominant immune complex material in rheumatoid arthritis (C4, Gl, K17, M4, M26, N5, Sll, W21, W22). The primary cause of rheumatoid factor production in rheumatoid arthritis is unknown. However, rheumatoid factors are known to be present in other diseases associated with chronic antigenic stimulation (C14, M14) and can be induced in vitro by stimulation with antigens, autologous aggregated IgG, anti-idiotype reagents, and polyclonal B cell activators such as lipopolysaccharide and Epstein-Barr virus (C4, Dll, F6, F7, Gil, 16, P10, S24). Rheumatoid factors, including IgG rheumatoid factors which form selfassociating intermediate-sized (11-19 S) complexes, play a major role in... 

Freund s adjuvant) used with an antigen to improve the immune response (antibody formation secondary to B-cell activation). Incomplete Freund s adjuvant does not contain the bacterial cells and is used to avoid an inflammatory response. See White, R.G., Factor affecting the antibody response, Br. Med. Bull. 19, 207-213, 1963 White, R.G., Antigen adjuvants, Mod. Trends Immunol. 2, 28-52, 1967 Myrvik, Q.N., Adjuvants, Ann. N.Y. Acad. Sci. 221, 324-330, 1974 Osebold, J.W., Mechanisms for action by immunologic adjuvants, J. Am. Vet. Med. Assoc. 181, 983-987, 1982 Warren, H.S., Vogel, F.R., and Chedid, L.A., Current status of... 

Figure 33.19. B-Cell Activation. The binding of multivalent antigen such as bacterial or viral surfaces links membrane-bound IgM molecules. This oligomerization triggers the phosphorylation of tyrosine residues in the ITAM sequences by protein tyrosine kinases such as Lyn. After phosphorylation, the ITAMs serve as docking sites for Syk, a protein kinase that phosphorylates a number of targets, including transcription factors.

Aversa, G., Punnonen, J. and de Vries, J.E. (1993b). The 26-kD ttansmembrane form of tumor necrosis factor alpha on activated CD4 T cell clones provides a costimulatory signal for human B cell activation. J. Exp. Med. 177, 1575-1585. 

Coffman, RL., Ohara, J., Bond, M.W. et. al. (1986). B cell stimulatory factor-1 enhances the IgE response of lipopolysaccharide-activated B cells. J. Immunol. 136, 4538-4541. 

Soluble factors, such as lymphokines and monokines, produced by T cells and monocytes, respectively, influence B-cell activation. Thymocytes also produce soluble factors which stimulate and support growth of B cells in vitro (Andersson et al., 1977). This forms the basis for the in vitro immunization and production of monoclonal antibodies (Reading, 1982). Soluble factors can be specific or nonspecific for the antigen (Volkman and Fauci, 1981). The antigen-specific factor may represent secreted T-cell receptors. Some monokines may also replace lymphokines in the immunization procedure in vitro (Jonak and Kennett, 1982). 

Vassalli P The pathophysiology oftumor necrosis factors. Annu Rev Immunol 1992 10 411 452. Florquin S, Amraoui Z, Goldman M Persistent production of TH2-type cytokines and polyclonal B cell activation after chronic administration of staphylococcal enterotoxin B in mice. JAutoimmun 1996 9 609-615. 

Fig. 4. The role of cytokines in controlling cellular interactions involved in the immune and inflammatory responses. In an immune response, ceils present antigens and release IL-1 to activate appropriate T-helper cells and lL-6, which acts as a B-cell differentiation factor. Activated T-helper cells produce a variety of cytokines, including lymphocyte growth (lL-2 and lL-4) and differentiation (IFNy and IL-10) factors and hemopoietic growth factors (IL-3 and GM-CSF). Macrophages can also be activated by antigen nonspecific mitogens such as LPS. Cytokines released include those with proinflammatoiy activities such as IL-ip, TNFa, and IL-8, as well as the anti-inflammatory IL-6.

C37. Crawford, R. M., Finbloom, D. S., Ohara, J., Paul, W. E., and Meltzer, M. S. B cell stimulatory factor-1 (interleukin-4) activates macrophages for increased tumoricidal activity and expression of la antigens. 7. Immunol. 139, 135-141 (1987). 

Penicillamine (250 mg p.o. q.i.d. 30 to 60 minutes before meals), a metal-chelating agent, is indicated in Wilson s disease, in cystinuria, in rheumatoid arthritis, and in heavy-metal poisoning. Penicillamine depresses circulating IgM rheumatoid factor (but not total circulating immunoglobnlin levels) and depresses T-cell, but not B-cell, activity. It also depolymerizes some macroglobulins (for example, rheumatoid factors). 

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