INFECTION of CD4⁺ T cells by human immune deficiency virus-1 (HIV-1) causes severe dysfunction of cellular immunity^1–3, but paradoxically results in intense polyclonal activation of B cells, possibly accounting for both hypergammaglobulinaemia and frequent development of B-cell malignancies seen in HIV-infected patients^4–7. We have reported that human CD4⁺ T-cell clones infected with HIV in vitro markedly stimulate immunoglobulin synthesis by B cells through a non-cognate, contact-dependent mechanism⁸. We show here that HIV-infected T-cell clones do not express the CD40 ligand (CD40L), a molecule critical for non-cognate B-cell activation⁹, but a small proportion of them do express membrane tumour-necrosis factor (TNF)-α. The ability of HIV-infected T-cell clones to induce polyclonal B-cell activation appears to be restricted to TNF-α-positive T blasts and is inhibited by antibodies against both TNF-α and TNF-α receptor. Freshly isolated CD4⁺ T cells from HIV-infected individuals express TNF-α on the cell membrane and induce TNF-α-mediated immunoglobulin production by B cells. Thus, membrane TNF-α seems to be involved in the polyclonal B-cell activation induced by HIV-infected T cells.