Literature DB >> 3509924

Activation of murine B cells from different tissues with different mitogens. II. Isotype distribution of secreted immunoglobulins in the presence and absence of IL-4-containing T cell supernatants.

A Bossie1, K H Brooks, P H Krammer, E S Vitetta.   

Abstract

In the accompanying report, we have compared a B cell-specific protein mitogen, Salmonella thyphimurium mitogen (STM), to lipopolysaccharide (LPS), dextran sulfate (DxS), and the combination of LPS/DxS with regard to their ability to induce B cell proliferation and differentiation. The results of these studies demonstrated that STM, LPS, and LPS/DxS induce significant expression of cytoplasmic immunoglobulin (Ig). In this report, we have analyzed the distribution of isotypes induced by each of these mitogens in the presence or absence of interleukin-4 (IL-4) containing T cell supernatants (SN), since IL-4 increases the secretion of IgG1 and IgE and decreases the secretion of IgG3 and IgG2b in LPS-stimulated splenic B cells. These experiments were designed to determine whether LPS was unique in its ability to "program" B cells to respond to IL-4 by secreting IgG1, as has been suggested in our previous studies. The current experiments also addressed the issue of whether splenic B cells were unique in their response to IL-4 by using B cells from other tissues. The efficiency of induction of cytoplasmic Ig measured in the preceding report was STM greater than LPS/DxS greater than LPS. DxS did not induce a significant level of cell proliferation, cytoplasmic Ig, or secreted IgM and inhibited the LPS-induced IgM response by approximately 50%. In contrast, STM induced an extremely high level of IgM secretion in splenic B cells. In this report, we demonstrate that the addition of IL-4-containing T cell SN to splenic B cells stimulated with LPS, LPS/DxS or STM increased the level of IgG1 and reduced the level of IgM, IgG3, and IgG2b secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1987        PMID: 3509924

Source DB:  PubMed          Journal:  J Mol Cell Immunol        ISSN: 0724-6803


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