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Khan, N. and Ghousunnissa, S. and Jegadeeswaran, S.M. and Thiagarajan, D. and Hasnain, S.E. and Mukhopadhyay, Sangita (2007) Anti-B7-1/B7-2 antibody elicits innate-effector responses in macrophages through NF- B-dependent pathway. International Immunology, 19 (4). pp. 477-486. ISSN 0953-8178

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Blocking T cell co-stimulatory signals by anti-B7-1/B7-2 mAb is an attractive approach to treat autoimmune diseases. However, anti-B7-1/B7-2 mAb treatment is known to exacerbate autoimmune diseases through mechanisms not fully understood. Tumor necrosis factor alpha (TNF-α) and reactive oxygen species (ROS) also play important roles in determining the clinical outcome of autoimmune diseases. In this study, we demonstrate that the anti-B7-1 and the anti-B7-2 mAbs activate macrophages for higher induction of TNF-α and other effector responses such as bacterial cytotoxicity and production of ROS. Nuclear factor-kappaB (NF-κB) was found to be increased with anti-B7-1/B7-2 mAb treatment. Inhibition of NF-κB activity by over-expression of phosphorylation-defective I-kappaB alpha in anti-B7-1/B7-2 mAb-treated macrophages decreased TNF-α production. These data indicate that anti-B7-1 and anti-B7-2 mAbs can trigger innate-effector responses in macrophages by activating NF-κB-signaling pathway. Our results suggest that the B7 molecules are not only essential for induction of adaptive immune responses but also play roles in activation of innate immune responses

Item Type: Article
Depositing User: Dr P Divakar
Date Deposited: 18 Aug 2015 11:01
Last Modified: 21 Aug 2015 04:29
URI: http://cdfd.sciencecentral.in/id/eprint/356

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