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T cells orchestrate adaptive immune responses by recognizing short peptides derived from pathogens, and by distinguishing them from self-peptides. To ensure the latter, immature T cells (thymocytes) diffuse within the thymus gland, where they encounter an ensemble of self-peptides presented on (immobile) antigen presenting cells. Potentially autoimmune T cells are eliminated if the thymocyte binds sufficiently strongly with any such antigen presenting cell. We model thymic selection of T cells as a random walker diffusing in a field of immobile traps that intermittently turn 'on' and 'off'. The escape probability of potentially autoimmune T cells is equivalent to the survival probability of such a random walker. In this paper we describe the survival probability of a random walker on a d-dimensional cubic lattice with randomly placed immobile intermittent traps, and relate it to the result of a well-studied problem where traps are always 'on'. Additionally, when switching between the trap states is slow, we find a peculiar caging effect for the survival probability. [ABSTRACT FROM AUTHOR]

Discusses a paper by G. Willimsky and T. Blankenstein which showed that sporadic tumors in mice, against which the immune system initially reacts, nevertheless manage to spread by molding the killer T cells into a state that tolerates them. Implications for the debate on whether the development of sporadic, nonviral tumors is really affected by so-called immunoediting; Concurrence of both sides of the controversy that both virus-induced and sporadic tumors do elicit immune responses, and that T-cell responses protect against viral carcinogenesis; Variation in the natural ability of tumors to activate dendritic cells; Need for tumors to be sensed by an exquisitely sensitive sentinel system, the dendritic cell network.