Experimental allergic encephalomyelitis (EAE), an animal model resembling multiple sclerosis (MS), is mediated by myelin antigen‐specific CD4+ T cells secreting cytokines such as interferon‐γ (IFN‐γ), tumor necrosis factor‐β (TNF‐β), and the proinflammatory cytokine TNF‐α—all associated with the T‐helper‐1 (Th1) T cell subset. Based on numerous similarities between MS and EAE, it has been postulated that Th1‐like T cells are involved in the pathogenesis of MS. Production of proinflammatory cytokines such as IFN‐γ and, in particular, TNF‐α/β by autoreactive T cells is considered crucial for the initiation and amplification of inflammatory brain lesions and possibly also for direct myelin damage. In contrast, regulatory cytokines such as interleukin‐4 (IL‐4), IL‐10, and IL‐13, which are associated with the Th2‐like phenotype, may play a role in the resolution of relapses. Although the human T cell response to myelin basic protein (MBP) is well characterized in terms of antigen specificity, HLA restriction, and T cell‐receptor (TCR) usage, little is known about the cytokine pattern of these autoreactive T cells. To gain such information, conditions for studying cytokine secretion by human autoreactive T cell clones (TCC) were established. The cytokine secretion profile of human autoreactive CD4+ TCC, specific for myelin basic protein peptide (83–89) [MBP(83–99)], a candidate autoantigen in MS, was investigated. Our results show that TCC cytokine production in long‐term culture was stable. In addition, the correlation of various cytokines within specific TCC revealed differences compared to murine T cells. The comparison of 30 human MBP(83–99)‐specific TCC demonstrated heterogeneity in cytokine secretion, with a continuum between Th1‐ and Th2‐like cells rather than distinct Th1 or Th2 subsets. These data are important for further investigation of the potential role of cytokines in the inflammatory process of MS, and provide a powerful tool to investigate therapeutic interventions with respect to their influence on cytokine secretion of autoreactive T cells. © 1996 Wiley‐Liss, Inc.