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J. Biol. Chem., Vol. 282, Issue 26, 18671-18675, June 29, 2007

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Eis (Enhanced Intracellular Survival) Protein of Mycobacterium tuberculosis Disturbs the Cross Regulation of T-cells^*

From the Drug Target Discovery and Development Division, Central Drug Research Institute, Chattar Manzil Palace, Lucknow 226001, U.P. India

The pathogenesis of tuberculosis is complex and its manifestations diverse, reflecting a lifetime of dynamic interactions between mycobacterial virulence factors and the human immune system. The pathogenic mycobacteria have developed strategies to circumvent the major killing mechanisms employed by macrophages and take advantage of the enclosed environment within its host cell to avoid humoral and cell-mediated immune responses. Secretory proteins play a major role in host-pathogen interactions. The eis (Rv2416c) gene has been identified as a secretory protein, and it has been shown that it enhances intracellular survival of Mycobacterium semgmatis in the macrophage cell line. The main aim of this study was to gain insight into the biological role of Eis in the host. Stimulation of T-cells with Eis recombinant protein of Mycobacterium tuberculosis inhibits Con A-mediated T-cell proliferation in vitro. Treatment of T-cells with Eis inhibits ERK1/2, JAK pathway, and subsequent production of tumor necrosis factor- and interleukin-4. On the contrary, there is increased production of interferon- and interleukin-10, which indicates that immunity in response to Eis treatment is skewed away from a protective T_H1 response and Eis disturbs the cross regulation of T-cells.

Received for publication, October 31, 2006 , and in revised form, April 10, 2007.

^* This work was supported by Grants MLP 0011 from the Central Drug Research Institute (CDRI) and SMM003 from the Council of Scientific and Industrial Research (CSIR). The CDRI communication number for this manuscript is 7091. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains two supplemental figures.

¹ A recipient of a Senior Research Fellowship from the Council of Scientific and Industrial Research, New Delhi, India.

² To whom correspondence should be addressed. Tel.: 91-522-2621411-418 (ext. 4380); 91-941-5409471; Fax: 91-522-2623938/2614217/2629504/2623405; E-mail: chash71{at}yahoo.com.

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