非肥胖型糖尿病的CD4淋巴细胞增多症定位在17号染色体上主要组织相容性复合体（MHC）基因座之外。

Nonobese diabetic CD4 lymphocytosis maps outside the MHC locus on chromosome 17.

作者信息

Koarada Syuichi, Wu Yuehong, Yim Young-Sun, Wakeland E W, Ridgway William M

机构信息

Division of Rheumatology and Immunology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.

出版信息

Immunogenetics. 2004 Aug;56(5):333-7. doi: 10.1007/s00251-004-0702-1. Epub 2004 Aug 12.

DOI:10.1007/s00251-004-0702-1

PMID:15309345

Abstract

Genetic control of homeostasis of peripheral CD4+ lymphocyte levels is incompletely understood. Recent genome scans have linked mouse peripheral CD4 levels to chromosome 17, with strongest linkage to the Ea region. Nonobese diabetic (NOD) mice demonstrate peripheral T-cell lymphocytosis, and previous studies also suggested that the MHC region might control this phenotype. Here we confirm that loci on Chr 17 control NOD peripheral CD4 lymphocytosis. An elevated NOD CD4:CD8 ratio maps to the same region, and we show it is due to increased numbers of CD4+ cells. However, using NOD MHC congenic mice, we demonstrate that the MHC region is excluded, and that NOD peripheral lymphocytosis is controlled by genetic intervals adjacent to the MHC region on Chr 17.

摘要

外周CD4+淋巴细胞水平稳态的遗传控制尚未完全明确。最近的全基因组扫描已将小鼠外周CD4水平与17号染色体联系起来，其中与Ea区域的连锁最强。非肥胖糖尿病（NOD）小鼠表现出外周T细胞淋巴细胞增多症，先前的研究也表明MHC区域可能控制这种表型。在此，我们证实17号染色体上的基因座控制NOD外周CD4淋巴细胞增多症。升高的NOD CD4:CD8比值定位于同一区域，并且我们表明这是由于CD4+细胞数量增加所致。然而，使用NOD MHC同源基因小鼠，我们证明MHC区域被排除在外，并且NOD外周淋巴细胞增多症由17号染色体上与MHC区域相邻的遗传区间控制。