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Sci. USA. 98:9243–48 Levine MH, Haberman AM, Sant’Angelo DB, Hannum LG, Cancro MP, Janeway CA Jr, Shlomchik MJ. 2000. A B-cell receptor-specific selection step governs immature to mature B cell differentiation. Proc. Natl. Acad. Sci. USA 97:2743–48 Jerne NK. 1974. Towards a network the- 27. 28. 29. 30. ory of the immune system. Ann. Immunol. (Paris) 125C:373–89 Sakato N, Janeway CA Jr, Eisen HN. 1977. Immune responses of BALB/c mice to the idiotype of T15 and of other myeloma proteins of BALB/c origin: implications for an immune network and antibody multispecificity.

This hypothesis has implications for the development of new strategies for tumor immunotherapy, as one would predict that blockade of PD-1/PD-L interactions could enhance tumor-specific T cell responses. ATTENUATION OF IMMUNE RESPONSES BY THE PD-1/PD-L PATHWAY Identification of the PD-1 ligands, PD-L1 (B7-H1) and PD-L2 (B7-DC), and assessment of their interaction with PD-1 confirmed the negative regulatory function of PD-1 in immune responses (71, 72). Neither PD-L1 nor PD-L2 bound to CD28, 4 Feb 2002 11:14 Annu.

88) also noted that the myelin protein MOG has homology with B7-1, B7-2, and butyrophilin, although MOG contains only an IgV extracellular domain. MOG is an autoantigen in EAE, and immunization of susceptible rats with the IgV domain of butyrophilin also results in an inflammatory response in the CNS due to cross-reactivity of T cells to MOG-derived epitopes (94). MOG maps to 6p21 in humans, centromeric to the butyrophilin genes and telomeric from the class I and II gene clusters (95, 96). Although MOG can act as an autoantigen in animal models of multiple sclerosis, as yet there are no data defining an interacting protein for MOG, nor any data implicating MOG as a costimulatory protein in immune function.

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