SummaryWe have previously reported that T cells bearing T cell receptors (TCRs) of 3`//$ type appear at a relatively early stage of primary infection with Listeria monocytogenes in mice. To characterize the early-appearing 3`//$ T cells during listeriosis, we analyzed the specificity and cytokine production of the 3`//$ T cells in the peritoneal cavity in mice inoculated intraperitoneally with a sublethal dose of L. monocytogenes. The early-appearing 3'//$ T cells, most of which were of CD4-CD8-phenotype, proliferated and secreted IFN-3' and macrophage chemotactic factor in response to purified protein derivative from Mycobacterium tuberculosis, or recombinant 65-kD heat-shock protein derived from M. bov/s but not to heat-killed Listeria.

Objective: To characterize the initiation and progress of localized autoimmune damage in Sjögren's syndrome (SS), an autoimmune disease that is also considered to be a lymphoaggressive disorder, by examining the pattern of cytokine production at the site of autoimmune damage. Methods. Using a polymerase chain reaction–based method, cytokine messenger RNA (mRNA) expression in the labial salivary glands of 15 patients with SS was investigated. In addition, the infiltrating lymphocytes in the labial salivary glands were examined immunohistochemically. Results. Messenger RNAs of Th1 cytokines, such as interleukin‐2 (IL‐2) and interferon‐γ, were consistently detected in all patients, while Th2 cytokine mRNAs, such as IL‐4 and IL‐5, were detected in some cases, in association with strong B cell accumulation in the labial salivary glands. Other cytokine mRNAs produced by a variety of cell types, including ILIO, IL‐6, and transforming growth factor β (TGFβ), were also consistently detected in all patients, while IL‐12 mRNA was detected in some of the patients. Conclusion. These results suggest that Th1 cytokines, as well as IL‐10, IL‐6, and TGFβ, are essential in the induction and/or maintenance of SS, while Th2 cytokines are involved in the progression of the disease process, especially local B cell activation.

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Three possible mechanisms have been proposed to explain development and maintenance ofT cell tolerance to self antigens : the inactivation of self-reactive lymphocytes (clonal anergy), their chronic suppression (clonal suppression), and their elimination (clonal deletion) (1, 2). Experimental attempts to prove these three possibilities have been severely limited because of the technical difficulties (2). A more direct approach to assess the cellular basis of tolerance induction, however, is now available by using the fact that the usage of a certain TCR Vo domain is strongly correlated with the reactivity to specific antigens (3-5). By exploiting such correlations, it has been demonstrated that self-tolerance to the products encoded by the Mls-1a allele (4, 5) or the Mls-2a allele (6, 7) is mediated via the clonal deletion of the self-reactive T cell clones .As to tolerance induction to allogeneic antigens, many attempts have been experimentally made . Those include neonatally induced tolerance (8), irradiationinduced tolerance (9-11), and antilymphocyte serum-induced tolerance (12, 13). Recently, MacDonald et al. (14) have indicated that neonatally induced tolerance to Mls-la-encoded antigens was likewise accompanied by the intrathymic elimination of V06-bearing cells, which are capable of recognizing Mls-1a-encoded antigens bound to MHC class II molecules, thus supporting the clonal deletion model. On the other hand, Qin et al. (15) have raised the possibility that tolerance to allograft induced by combining bone marrow transplantation (BMT)1 together with administration of CD4 and CD8 mAb in adult mice is, at least in part, due to clonal anergy rather than deletion . Thus, the underlying mechanisms in the development and maintenance of the donor-specific transplantation tolerance still remain controversial .We have previously reported a method of allo-tolerance induction in adult mice

SUMMARYThe relative contribution of polymorphonuclear leukocytes and macrophages in the early protection against intranasal infection of mice with influenza virus was investigated. Virus multiplication in the lung in the early phase of infection with less than 1.5 x 10 3 plaque-forming units was enhanced by X-ray irradiation. The intranasal administration of carrageenan did not influence the titre of virus. However, when mice were infected with 1.5 x 10 4 plaque-forming units, the virus titre was elevated by intranasal administration of carrageenan as well as by X-ray irradiation, but not by intraperitoneal administration of carrageenan. The intranasal administration of carrageenan not only inhibited the phagocytic activity of alveolar macrophages but also enhanced susceptibility to the virus. On the other hand, polymorphonuclear leukocytes were capable of phagocytosing the virus in vitro and were non-permissive for virus infection. Neutralizing antibody and interferon were not detectable in the early stage of the infection. These results suggested that polymorphonuclear leukocytes (Xray-sensitive, carrageenan-resistant) were the cells primarily responsible for early protection in influenza virus infection and that after infection with a high dose of the virus alveolar macrophages (X-ray-resistant, carrageenan-sensitive) also played a protective role in the early phase.