Hepatic granulomatous lesions were induced in mice by a single intraperitoneal injection of 3 mg of disrupted Streptococcus pyogenes cell-wall material. Mice carrying the H-2b or H-2k haplotypes were highly susceptible to the induction and three weeks after the injection produced numerous granulomas
Genetic control of mitogen-induced B-cell hyperproliferation in SM/J mice
β Scribed by Roslyn Stone; David Engel
- Publisher
- Springer-Verlag
- Year
- 1985
- Tongue
- English
- Weight
- 374 KB
- Volume
- 22
- Category
- Article
- ISSN
- 0093-7711
No coin nor oath required. For personal study only.
β¦ Synopsis
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 x SM)F1, F 2 and (F 1 x 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 It-2 major histocompatibility complex.
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