Abstract
Abstract The lupus-susceptibility (278-37)rec1 sublocus is derived from the NZB-derived Sle2 locus found in the NZM2410 lupus-prone mouse. Our previous results showed that the candidate gene p18 in the (278-37)rec1 sublocus demonstrated significantly reduced mRNA expression and the (278-37)rec1 sublocus enlarged spleen, more notably peripheral lymph nodes in Fas-deficient mice. Our current research discovered firstly that the mouse with both p18 gene deletion and lpr mutation displayed expanded peripheral lymph organs as the same as the B6.(278-37)rec1.lpr mouse, meaning an association of p18 deficiency and lymphocyte hyperproliferation. Secondly, the B6.(278-37)rec1.lpr mouse showed significantly more Ki67+ T cells in lymph nodes than B6.lpr mouse, but T cells from both B6.(278-37)rec1.lpr and B6.lpr mice have the same proliferation response in vitro with stimulation by anti-CD3 and anti-CD28. Furthermore, both Treg cell percentage and the ration of Treg/T effective cell in B6.(278-37)rec1.lpr mouse showed markedly decreased in spleen and lymph nodes compared with B6.lpr mouse, but both mouse stains have the same Treg function in inhibiting T cell proliferation. Finally, the T cell apoptosis of B6.(278-37)rec1.lpr mouse seems unimpaired in activation-induced cell death assay. In summary, the T cell hyperproliferation controlled by the (278-37)rec1 sublocus involves several mechanisms, but their interrelation needs further to be elucidated in the future.
Published Version
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