Cavaleiro, R.Brunn, G. J.Albuquerque, A. S.Victorino, R. M.Platt, J. L.Sousa, A. E.2015-06-172015-06-172007Eur. J. Immunol. 2007. 37: 3435–34440014-2980http://onlinelibrary.wiley.com/doi/10.1002/eji.200737511/fullhttp://dx.doi.org/ 10.1002/eji.200737511http://hdl.handle.net/10451/18304© 2007 WILEY-VCH Verlag GmbH & Co. KGaA, WeinheimHIV-2 is associated with an attenuated form of HIV disease. We investigate here the immunosuppressive effects of the HIV-2 envelope protein, gp105. We found that gp105 suppresses activation of T cells through a monocyte-mediated mechanism. Suppression of T cell activation by gp105 depends on contact between monocytes and T cells, but not on CD4+CD25+ T cells. The TLR4 pathway is likely involved, since gp105 activates TLR4 signaling and induces TNF-α production by monocytes. Immunosuppression is viewed as the main pathophysiologic consequence of infection by HIV. However, the main immunologic defect caused by HIV, depletion of T cells, requires T cell activation. Our findings are consistent with a new concept that HIV-2 envelope proteins act on monocytes to suppress T cell activation and that this property may contribute to the benign course of HIV-2. We hypothesize that the HIV-2 envelope immunosuppressive properties limit bursts of T cell activation, thus reducing viremia and contributing to the slow rate of disease progression that characterizes HIV-2 disease.engHIVHost/pathogen interactionsImmunopathologyMonocytesToll-like receptorsjournal article