Summary
The present study has examined a functional role of Ia molecules expressed on murine B cells in polyclonal B cell differentiation induced by lipopolysaccharide (LPS). Reverse IgM PFC responses of unprimed B cells induced by LPS in the apparent absence of T cells and adherent accessory cells were markedly inhibited in a haplotype-specific manner by Fab monomer fragment of anti-class II (Ia) but not anti-class I MHC monoclonal antibody (mAb). However, the degree of inhibition of LPS responses of H-2-heterozygous F1 B cells expressing both parental I-A products by either one of anti-I-A mAb was at best half that of the parental B cells. Interestingly, when (B10 × B10.- BR)F1 (H-2b/k) B cells were fractionated into adherent and nonadherent populations by their ability to bind to parental B10 B cell monolayers, LPS responses of Fl B cells adherent to and nonadherent to the FO B cell mono-layers were selectively inhibited by anti-I-Ab and anti-I-Ak mAb, respectively. These results suggest that LPS-responsive F1 B cells comprise at least two separate populations with restriction specificity for only one of the parental I-A products expressed on B cells. In addition, it was demonstrated that the I-A-restriction specificity of LPS-responsive B cells is “plastic” and determined by H-2-genotype of bone marrow cells present during B cell ontogeny but not by that of radiation-resistant host elements. Namely, the LPS responses of B10-derived B cells from (B10 + B10.BR) (H-2b × H - 2k)F1 radiation bone marrow chimeras but not from B10 (H-2b × H-2k)F1 chimeras became sensitive to the inhibition of anti-I-Ak mAb in the presence of mitomycin C-treated I-Ak-positive B cells, supporting a notion of receptor-Ia molecules interactions rather than like-like interactions. Thus, the present results provide evidence indicating that B-B cell interaction via recognition of self-I-A products is a crucial event in the polyclonal B cell differentiation induced by LPS.
This work was supported by Grant-in-Aids from the Ministry of Education, Science and Culture, and the Osaka Foundation for Promotion of Clinical Immunology.
Fellowship of the Japan Society for the Promotion of Science for Japanese Junior Scientists.
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Takahama, Y., Ono, S., Ishihara, K., Muramatsu, M., Hamaoka, T. (1990). Involvement of I-A-Restricted B-B Cell Interaction in the Polyclonal B Cell Differentiation Induced by Lipopolysaccharide. In: Friedman, H., Klein, T.W., Nakano, M., Nowotny, A. (eds) Endotoxin. Advances in Experimental Medicine and Biology, vol 256. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-5140-6_40
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