EDITORIAL The Thymus and Lymphoid Proliferation

I N THIS ISSUE, a review is presented by Arnason, Jankovic and Waksman on some of the functions of the thymus gland, bearing particularly upon its relation to lymphocytes and immune reactions. This gland, long known as an obscure collection of lymphoid or paralymphoid cells, has recently jumped into prominence as possibly the “master gland” controlling the immune response. Jacques Miller,’ working at Chester Beatty Institute in London, and Robert Good2 and his group of Minneapolis have demonstrated that thymectomized newborn mice are unable to respond effectively to antigenic stimulation, either in the form of skin transplants or of soluble antigens. Miller demonstrated that the lymphocyte:granulocyte ratio in thymectomized mice was reduced and that a conspicuous deficiency of the germinal centers of lymph nodes developed. Previously ( 1956 ) Metcalf’s experiments3 had indicated the presence of a lymphocyte stimulating factor (LSF ) in the thymus. From these various observations, it could be postulated that the thymus had a controlling action upon the production of lymphocytes. In a recent publication, Burnet4 discussed the possibility that the thymus gland produced “first level” lymphocytes which were immunologically tincommitted, but that when these cells lodged in suitable tissues such aS lymph nodes and spleen, they had the possibility of becoming committed to specific antibody production, when stimulated by antigen. This was quite a reversal for Bumet, whose clonal selection hypothesis had indicated that at birth or shortly thereafter all immunologically competent cells were already committed to the production of single antibodies in response to single, specific antigens. Thus, the antigen, when it entered the body, would wander about until it found its predestined specific clone of immunocompetent* cells or immunocytes. This Jerne-Bumet concept of multitudes, or in less drastic terms of perFlaps hundreds, of gentically determined clones of antibody producing cells which could react specifically only to specific antigens was, it must be confessed, a bit difficult to swallow. Fortunately, Burnet’s recent work with the Bielschowsky strain (NZB/BL) of New Zealand mice,4’5 having a genetically determined autoimmune hemolytic anemia, led him to modify his theory considerably. These unusual mice presented the investigator with the first opportunity to study a spontaneously developing autoimmune disease in the experimental animal. Highly inbred mice of this strain, first discovered by the Bielschowskys and studied by Helyer and Howie at the University of Otago in New Zealand, developed the characteristic features of auto-