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ß₂-Microglobulin-Dependent T Cells Are Not Necessary for Alloantigen-Induced Th2 Responses After Neonatal Induction of Lymphoid Chimerism in Mice¹

Institut National de la Santé et de la Recherche Médicale (INSERM) U.28, Université Paul Sabatier, Hôpital Purpan, Toulouse Cedex, France

We have analyzed the requirement for ß₂-microglobulin (ß₂m)-dependent T cells in the generation of allogeneic Th2 responses in vivo. A neonatal injection of semiallogeneic cells in BALB/c mice induces a state of chimerism that promotes the differentiation of donor-specific CD4⁺ T cells toward the Th2 phenotype. Polyclonal T-B cell interactions occur in this model between host Th2 and donor B cells, resulting in the production of IgE Abs. IgE production and Th2-priming are critically dependent upon the early production of IL-4. Our data in the present paper demonstrate that: 1) IgE synthesis and the up-regulation of MHC class II and CD23 molecules on B cells are independent of ß₂m expression in the host, 2) no difference in the induction of CD4 alloreactive Th2 cells could be observed between ß₂m^-/- and their wild-type control littermates when Th2-priming was measured in adult mice, and 3) the Th2 response and IgE production is induced in the complete absence of ß₂m-dependent T cells both in the host and in the inoculum. Therefore, using a variety of assays, we could not demonstrate diminished responses in mice with a disrupted ß₂m gene in this model of Th2-mediated allogeneic interaction, indicating that ß₂m-dependent NK1.1⁺ and CD8⁺ T cells are not required for the generation of alloreactive Th2 responses in vivo.

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