Brines R, Lehner T
Clin Exp Immunol. 1987 Feb;67(2):398-405.
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.
在富含单核细胞的细胞存在的情况下，半抗原-载体偶联物二硝基苯-链球菌抗原（DNP-SA）可引发人T4+细胞作用于自身外周血B细胞的辅助功能。富含单核细胞的细胞的抗原呈递功能可被自身T8+野豌豆凝集素黏附细胞亚群（T8VV+）替代。细胞清除研究证实，T8VV+细胞的呈递是由T细胞介导的，因为用抗T3抗体和补体杀伤可去除T8VV+细胞的抗原呈递能力，但不能去除富含单核细胞的细胞的抗原呈递能力。此外，用抗Ia特异性单克隆抗体和补体杀伤可消除T8VV+细胞的抗原呈递，这表明后者表达一种Ia基因产物。抗原呈递对引发抗DNP IgM抗体的DNP-SA具有特异性，因为对破伤风类毒素无反应则不会产生抗DNP IgM抗体。我们认为，T细胞之间的相互作用不仅可能通过T4+细胞诱导T8+抑制细胞功能发生，还可能通过T8+细胞向T4+细胞呈递抗原以在无其他辅助细胞的情况下诱导辅助功能的反向活性发生。
