7th International AIDS Conference Florence, Italy — June 16-21, 1991

Int Conf AIDS 1991 Jun 16-21; 7:26 (abstract no. M.A.20)
Romagnani S, Macchia D, Parronchi P, Piccinni MP, Simonelli C, Ravina A, Mazzetti M, Santoni F, Maggi E; Istituto di Clinica Medica 3, Universita di Firenze (Italia)

OBJECTIVE: To examine the alterations induced by HIV-1 infection on the function of helper T cells with particular regard to their involvement in the polyclonal B cell response.

METHODS: In vitro infection with HIV-1 of PPD- or tetanus toxoid-specific CD4+ human T cell clones (TCC) derived from uninfected individuals. Assessment of HIV-1 infection of T cells by PCR and by the measurement of RT activity and p24 protein in TCC supernatants. Evaluation of the proliferative response, production of cytokines and helper activity for immunoglobulin (Ig) synthesis of HIV-1-infected TCC.

RESULTS: Human TCC infected in vitro with HIV-1 showed reduced ability to proliferate and to produce IL-2, IL-4 and IFN-gamma, but they exhibited enhanced ability to produce TNF-alpha. Furthermore, infection with HIV-1 enabled TCC to stimulate the synthesis of extraordinarily high amounts of IgM, IgG, and IgA in both autologous and allogeneic B cells in the absence of any stimulant. This helper effect was mediated by a physical contact between T and B lymphocytes.

CONCLUSIONS: These data demonstrate that in vitro infection with HIV-1 enables human CD4+ TCC to produce TNF-alpha and to stimulate Ig synthesis by B cells via an antigen-nonspecific, MHC-unrestricted, contact-dependent, mechanism. This may explain, at least in part, hypergammaglobulinemia and the other phenomena indicative of polyclonal B cell activation seen in HIV-1-infected individuals.

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