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• W2741128306 abstract "Navreet K. Nanda and Eli E. Sercan Department of Microbiology and Molecular Genetics University of California, Los Angeles Los Angeles, California 90024-1489 A quiet but profound revolution in theoretical framework, a paradigm shift, now has infused the consideration of therapies in autoimmune diseases and cancers, as exem- plified at the Jennifer Jones Simon Foundation workshop on Tumor Antigens as Self-Antigens, held in Los Angeles, California, on January 28-27, 1995. It is becoming accepted that a large set of antigenic determinants of the self have not induced self-tolerance (reviewed by Sercarz et al., 1993) and that these peptide determinants furnish target structures for autoimmune at- tack (reviewed by Lanzavecchia, 1995) and could provide potential targets for immune responses directed against tumors. It is not necessary to seek mysterious nonself- or neoself-antigens expressed by the tumor. The bulk of the lively and open discussion, characteristic of these free format workshops with no fixed presentations, was modu- lated very capably by A. Tobin (University of California, Los Angeles), a neurobiologist, and focused on how to initiate, maintain, and regulate antitumor autoimmunity, which could translate into effective treatment in cancer clinics. Are there in fact certain tumor-related determinants that can be rendered into crucial targets of attack by the im- mune system? The pertinent focus is on suitable antigen processing and subsequent presentation by major histo- compatibility complex (MHC) class I and class II molecules expressed by tumor cells. Any of the peptides that is bound in the groove of an MHC molecule on tumor cells provides a potential target determinant for attack by the immune system. The peptides bound by the MHC molecules of all ceils, including tumor cells, are derived from endogenous cellular (or viral) proteins, and the antigen-processing ma- chinery of the cells manages to display certain antigen determinants to ambient T cells. Tumor cells are distinct in that they possess additional oncoproteins that either are overexpressed owing to dysregulation or are mutated and have thereby conferred the tumor phenotype to these cells, to developmental antigens reexpressed during the process of tumorigenesis, or to passenger mutations in nononcogenic proteins that result from the loss of mecha- nisms that maintain genomic stability. Using T cell clones that are specifically able to kill the tumor as detectors for immunogenic tumor-derived determinants bound to MHC molecules of the tumor, several investigators have shown that T cells indeed recognize peptides from endogenous normal (and occasionally mutant) self-proteins. T. Boon and colleagues (van der Bruggen et al., 1991), in their pioneering studies, drew a page from bacterial genetics and cloned genes encoding tumor antigens recognized by CD8 T cells specific for human melanomas. Melanoma antigen 1 (MAGE-1) to MAGE-3 were the original family of human melanoma-specific antigens that were molecularly defined in this way and were followed by isolation of deter- minants on tyrosinase, gp100, and Melan-A-MART-1 rec- ognized by antimelanoma T cells (reviewed by Houghton, 1994). It is interesting that the MAGE gene family is not expressed in any normal adult tissue except testis, but is expressed in a large proportion of other human tumors (including small cell lung carcinoma, breast cancers, and colon carcinoma) and perhaps represents developmental antigens reexpressed during the process of tumorigene- sis. Tyrosinase, gplO0, and Melan-A-MART-1 are normal self-proteins specific to the melanocyte lineage and T cells specific for determinants on each of these antigens can be found in a large majority of melanoma patients (re- viewed by Houghton, 1994; Pardoll, 1994). It is thus be- coming clear that there is no special group of proteins that can be dubbed tumor antigens, and the distinction between self-antigens and tumor antigens is rapidly van- ishing. Thus, as summed up by Tobin, we have entered an era in which “we either know the tumor antigens or know how to know them.” But can the immune system make a T cell response against all the peptides bound to MHC molecules of a tumor cell? Part of the answer lies in the availability of the Tcell repertoire membership directed against MHC-bound determinants and the proportion of T cells rendered toler- ant in each individual. It is now thought that only well- expressed self-determinants are efficient in tolerance in- duction. In addition, on every self-antigen, there are sequestered determinants that do not succeed in inducing tolerance but that, under the circumstances of severe in- flammation and its attendant cytokine milieu, can be dis- played in an immunogenic context. Among the diversity of self-reactive T cells that evade negative selection, tu- mor-specific members can be mobilized under conditions of heightened awareness by the immune system-in which MHC molecules, surface adherence costimulators are up-regulated and become available for possibly killing interaction along with newly displayed, pre- viously “cryptic” self-antigenic determinants (reviewed by Sercarz et al., 1993; Lanzavecchia, 1995). Autoimmune disease on one hand and the existence of tumor-specific cytolytic T cells recognizing self-peptides in the cancer patient on theother are atestimonyto theenormouspoten- tial resources inherent in the positively selected T cell rep- ertoire, directed to the cryptic self. For example, T cells specific for peptides of self-protein tyrosinase can be iso- lated from normal individuals, which can attack and kill melanoma cells from human lymphocyte antigen (HLA)- matched cancer patients (Visseren et al., 1995). What may be critical is the density of the upregulated peptide MHC complexes, as well the expression of costimula- tory signals that influence activation of the otherwise silent tumor-specific T cell repertoire existent in the cancer pa- tient. The task at hand is how to generate and manipulate" @default.
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• W2741128306 title "Induction of Anti-Self-Immunity to Cure Cancer Meeting Review" @default.
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