B-cell mitogenic effect of dinitrophenyl derivative of Mycobacterium tuberculosis antigens

Prabhu, Anila ; Sarin, Apurva ; Saxena, Rajiv K. (1993) B-cell mitogenic effect of dinitrophenyl derivative of Mycobacterium tuberculosis antigens Cellular Immunology, 149 (2). pp. 422-432. ISSN 0008-8749

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Official URL: http://www.sciencedirect.com/science/article/pii/S...

Related URL: http://dx.doi.org/10.1006/cimm.1993.1167


Soluble antigens derived from the H37Ra strain of Mycobacterium tuberculosis (Ra antigen) induced marginal proliferative response in spleen cells from unsensitized mice. The FDNB derivative of this antigen (Ra-DNP), however, had a marked proliferation-inducing effect. An increase in the population of B-cells lint a reduction in the T-cell population was noted in Ra-DNP-treated spleen cell cultures. BSA-DNP derivatives used as control had no effect on mouse spleen cell proliferative activity. Moreover, addition of BSA-DNP along with Ra did not improve the proliferative response to the latter, indicating that in order to obtain proliferative activity, DNP residues must be present on Ra antigens themselves. Thymidine incorporation studies using sorted cell populations indicated that B-cells proliferated in response to Ra-DNP. The effect of Ra-DNP was neither blocked by Polymyxin-B treatment, nor retained by an endotoxin removal column, suggesting that lipopolysaccharide was not responsible for the B-cell mitogenic effect of Ra-DNP. As compared to Ra antigen, Ra-DNP derivative was found to bind more efficiently to B-cells as well as to mouse Ig. Additionally, lymph node cells derived from Ra-sensitized mice proliferated significantly better in response to Ra-DNP. These results indicate that FDNB derivatization of Ra antigen renders it more reactive with B-cells, which may in turn be responsible for a better T-cell reactivity of the derivative, since B-cells can act as antigen-presenting cells. It is possible that DNP residues may facilitate the interaction of Ra antigen with B-cells, perhaps through their Ig receptor.

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