Abstract
Previous studies have shown that B cells from SM/J mice exhibit hyperproliferative responsiveness to several bacterial-derived B-cell mitogens. This hyperresponse trait was found to be under autosomal, polygenic control by non-H-2 genes. We have now estimated the number of genes involved by statistical analysis of the proliferative responses of splenocytes from SM/J and low-responder C57BL/6J strains, and progeny from the (B6 × SM)F1, F2 and (F1 × B6) crosses. The number of loci involved was ascertained using two different statistical approaches. An estimate of two loci was determined using chi-squared statistics. The second approach, based on an additive model in the natural log scale, also pointed to a lower bound of two genes. We conclude that the hyperresponse to B-cell mitogens in SM/J mice is determined by two autosomal genes which are not linked to the H-2 major histocompatibility complex.
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Abbreviations
- LPS:
-
a bacterial lipopolysaccharide
- AVIS:
-
a mitogenic preparation from Actinomyces viscosus
- B6:
-
C57BL/6J mice
- 125IUdR:
-
125Iodo-deoxyuridine
References
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Stone, R., Engel, D. Genetic control of mitogen-induced B-cell hyperproliferation in SM/J mice. Immunogenetics 22, 69–75 (1985). https://doi.org/10.1007/BF00430595
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DOI: https://doi.org/10.1007/BF00430595