Immunoglobulin‐specific T‐B cell interaction

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Abstract
Immunoglobulin (Ig)‐specific T‐B cell interactions have been studied in the model of T cell recognition of the χ chain Igχ‐1b allotype in Igχ‐1‐congeneic rat strains. An efficient presentation of endogenous Ig allotypic determinants by irradiated spleen cells from (WAG.1b x August)F1 (RT‐1u/c; Igχ‐1b/1a) rats to Igχ;‐1b‐specific lymph node T cells from Igχ;‐1‐congeneic (WAG x August)F1 (RT‐1u/c; Igχ‐1a) rats was demonstrated. This presentation was found to be sensitive to high irradiation doses (WAG x 1000 rad). By fractionation of Igχ‐1b+ F1 spleen cells on Percoll density gradient we have shown that a radioresistant, low‐density fraction, consisting mainly of macrophages (MΦ) and dendritic cells, triggers only weak Igχ;‐1b‐specific T cell response. The high level of response was observed against radiosensitive spleen cell fractions of intermediate and high density, suggesting that B cells were the main antigen‐presenting cells (APC) of Igχ;‐1b determinants of endogenous Ig. This conclusion was confirmed in the experiments using purified B cells from Igχ;‐1b‐bearing rats. Earlier we have shown that the responsiveness of August (RT‐1c; Igχ;‐1a) and WAG (RT‐1u; Igχ;‐1a) rats to Igχ;‐1b in vivo is controlled by the dominant allele of an RT‐1‐linked Ir gene. August and (August x WAG)F1 rats were found to be responders to Igχ;‐1b while WAG rats were nonresponders. The same pattern of Ir gene‐controlled reactivity was demonstrated using an Igχ;‐1b‐specific T cell proliferation assay. Igχ;‐1b‐specific F1 T cell response was only observed when Igχ;‐1b+ B cells or IgG (Igχ;‐1b)‐pulsed Mϕ‐bearing responder major histocompatibility complex (MHC) haplotype were used as the APC. Anti‐RT‐1 monoclonal antibody inhibition studies suggested that the RT‐1Bc molecule is the main restricting element of T cell recognition of Igχ;‐1b+ B cell as well as exogenous IgG (Igχ;‐1b). We have demonstrated allelic exclusion of Igχ;‐1b presenting function by negatively and positively selecting for Igχ;‐1b+ and Igχ;‐1a+ B cells from heterozygous F1(Igχ;‐1b/la) rats. This clearly indicate that the B cells presented exclusively Igx‐1b allotypic determinants of their own Ig. Furthermore, it was found that Igχ;‐1b‐specific T cell activation was not caused by the in vitro transfer of Ig(Igχ;‐1b) molecules from one B cell to another, or to some residual APC of another type. Thus, B cells presented with high efficiency Igχ;‐1b determinants of self‐synthesized Ig in association with MHC class II molecule to Igχ;‐1b‐specific T cells.