DOES STRESS PRECIPITATE ATI'ACK S OF MULTIPLE SCLEROSIS? P. Nisipeanu and A.D. Korczyn, !chilov H,~pital. Sackle: School of Medicine, Tel- Aviv University, Tel-Aviv. It has been repeatedly claimed that stressful events may be relatc~ to clinical aggravation of multiple sclerosis (MS). We investigated the occurrence of re~apses in MS patients living in the central area of Israel in the period of missile attacks daring, the Gulf war (January 16- February 28, 1991), and in the following 3 months. Thirty two patients with relapsing/remitting clinically definite MS were instructed to report a possible relapse. Thr~ patients considered that a relapse had occurred, one in February and the other two in April. in all three patients, the clinical examination confirmed the worsening. This number of relapses does not exceed expectation. The role of psychological stress in precipitating clinical relapses in MS, needs further study, since various types of stress and different durations of stress may affect neurological outcome to a different degree. 139 HYPOTHESIS ON THE EXISTENCE OF SELF-SUPERVISED IMMUNE SURVEILLANCE Zvi Grossman, Dept. of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv, Israel Infection can, in theory, "sneak" through classical immunological surveillance if its propagation is gradual. Moreover, destructive immune response may be undesirable in the case of a slow but wide-spread infection. In that case, a different mode of resistance is required whereby patterns of signals are recognized, classified and evoke selective responses. It has been proposed that "specialized" subsets of T cells might respond to different infection-associated foreign and autologous antigens, such as stress proteins (HSP), in particular ways, for instance by direct activation, inactivation or destruction of their targets, or by relay of signals to other components of the immune system. It is further proposed that this "specialization" of T cells is not entirely preprogrammed but could emerge from a dynamic process and involve a degree of self organization based on "cellular learning'. Suppose that stressed cells secrete some short-lived "stress factor", whose variable concentration is a local measure of "stress" in the tissue, and that changes in this concentration bias the process of cell learning. In the adaptive network of mobile, loosely connected cells, adaptation of each element is driven by perturbations, which are partly due to fluctuations in local stress levels. The network self-organiz~ in attempt to minimize these levels or, equivalently, to improve its physiological performance.

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HYPOTHESIS ON THE EXISTENCE OF SELF-SUPERVISED IMMUNE SURVEILLANCE Zvi Grossman , Dept. of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv, Israel Infection can, in theory, "sneak" through classical immunological surveillance if its propagation is gradual. Moreover, destructive immune response may be undesirable in the case of a slow but wide-spread infection. In that case, a different mode of resistance is required whereby patterns of signals are recognized, classified and evoke selective responses. It has been proposed that "specialized" subsets of T cells might respond to different infection-associated foreign and autologous antigens, such as stress proteins (HSP), in particular ways, for instance by direct activation, inactivation or destruction of their targets, or by relay of signals to other components of the immune system. It is further proposed that this "specialization" of T cells is not entirely preprogrammed but could emerge from a dynamic process and involve a degree of self organization based on "cellular learning'. Suppose that stressed cells secrete some short-lived "stress factor", whose variable concentration is a local measure of "stress" in the tissue, and that changes in this concentration bias the process of cell learning. In the adaptive network of mobile, loosely connected cells, adaptation of each element is driven by perturbations, which are partly due to fluctuations in local stress levels. The network self-organiz~ in attempt to minimize these levels or, equivalently, to improve its physiological performance.