Peripheral blood γ-δ T cells lyse fresh human brain—Derived oligodendrocytes

✍ Scribed by Dr. Mark S. Freedman; Theodora C. G. Ruijs; Liisa K. Selin; Jack P. Antel

• Publisher: John Wiley and Sons
• Year: 1991
• Tongue: English
• Weight: 641 KB
• Volume: 30
• Category: Article
• ISSN: 0364-5134
• DOI: 10.1002/ana.410300608

✦ Synopsis

T cells are postulated to contribute to the injury of the oligodendrocyte-myelin complex underlying the demyelinating disease multiple sclerosis (MS). The apparent lack of class I or I1 major histocompatibility complex (MHC) expression in situ on human oligodendrocytes and the consistent failure to identify a universal myelin antigen in MS suggest that the immune damage might be mediated by effector T cells that are capable of reacting in an antigen-nonspecific and possibly MHC-unrestricted manner, such as T cells expressing the 7-6 T-cell receptor. Since y-6 T cells are reported to be present in MS plaques and an increased number are found in the cerebrospinal fluid of patients with MS, we directly examined whether y-6 T cells are capable of inducing injury to human oligodendrocytes. We found, using a 6-hour jlCr release assay, that oligodendrocytes cultured from surgically resected human brain specimens were effectively lysed in a dose-dependent manner by human y-6 T cells (28 k 5% mean specific lysis, n = 6, at an effector-target ratio of 20: 1). Although heat shock protein HSP72, a putative y-6 T-cell recognition molecule, could be induced in vitro in our oligodendrocytes, an antibody to HSP72 did not inhibit y-6 T cell-mediated lysis of oligodendrocytes. These results suggest that 7-6 T cells gaining entry into the central nervous system may be deleterious to oligodendrocytes and thus may contribute to the pathogenesis of MS.