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Lymphocyte function and the role of regulator cells in multiple Sclerosis

Although the etiology of multiple sclerosis (MS) remains unknown, evidence continues to accumulate pointing to aberrant immune function in this disease, both when the disease is active and during periods of its seeming quiescence. Classically, the immune system has been considered to be comprised of three major cell types: (1) thymus-derived lymphocytes (T cells), which are the effectors of cell-mediated immune responses; (2) bone-marrow derived lymphocytes (B cells), which act in antibody-mediated immune responses; and (3) cells of the monocyte-macrophage series. The standard classification oversimplifies the in vivo situation: Subclasses of T and B cells can now be delineated and evidence has been advanced for the existence of functional differences between macrophages harvested from different loci. The best studied of immunocyte subclasses are those of the T cells. Broadly, these can be divided into effector and regulator subgroups. Among regulator T cells are helper and suppressor subsets. The suppressor T-cell subset can be further subdivided into specific and nonspecific types. Specific suppressors are antigen triggered and suppress the response to a specific antigen. Nonspecific suppressors depress the immune response in toto. Study of specific suppressor cell function is not feasible in MS since no antigen specific for MS is known. On the other hand, nonspecific suppression can be studied in MS and, as will be shown, is markedly decreased when the disease is active. Helper T cells augment the magnitude of the immune response and suppressor T cells lessen it. At any moment the net immune response in vivo is a function of the balance between these countervailing forces. Thus, an immune response may be abrogated equally well by abolition of helper function or by augmentation of suppressor function. Given these considerations, current enthusiasm for cytotoxic immunosuppressive drugs as therapy in MS may be misdirected. Cytotoxic drugs depress both helper and suppressor cell populations and, if this occurs to a comparable extent in both cell populations, the effect on the net immune response may be zero. In animals, cyclophosphamide has been reported to selectively kill suppressor cells. 1,2 In consequence, use of this drug during flareups of MS might be contraindicated. Since MS is characterized by exacerbations and remissions, study of immune parameters which fluctuate with disease activity might offer clues t o the defect in immune regulation which permits attacks to occur or disease to progress. Manipulation-by chemical or pharmacologic means-of regulator cell functions which are abnormal when disease is active might blunt the severity of attacks of MS even while the fundamental cause of the disease itself remains unknown. The work on this problem currently being undertaken in our laboratories constitutes the theme of this paper.