The helper function of human T4+ cells acting on autologous peripheral blood B cells was elicited by the hapten-carrier conjugate DNP-streptococcal antigen (DNP-SA), in the presence of monocyte-enriched cells. The antigen presenting function of monocyte-enriched cells can be replaced by a subset of autologous T8+ Vicia villosa lectin adherent (T8VV+) cells. Cell depletion studies confirmed that the T8VV+ cell presentation was mediated by a T cell since killing with anti-T3 antibody and complement removed the antigen presenting capacity of T8VV+ cells but not of monocyte-enriched cells. Furthermore, killing with anti-Ia specific monoclonal antibody and complement abrogates antigen presentation by the T8VV+ cells, suggesting that the latter express an Ia gene product. The antigen presentation is specific to DNP-SA which elicits anti-DNP IgM antibodies, as the latter are not produced in response to tetanus toxoid. We suggest that interactions between T cells may occur not only by T4+ cells inducing T8+ suppressor cell functions but also the reverse activity of T8+ cell presenting antigen to T4+ cells to induce helper function in the absence of other accessory cells.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1542583 | PMC |
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