Chambers C A, Sullivan T J, Allison J P
Howard Hughes Medical Institute, Department of Molecular and Cellular Biology, University of California, Berkeley 94720, USA.
Immunity. 1997 Dec;7(6):885-95. doi: 10.1016/s1074-7613(00)80406-9.
CTLA-4-deficient animals develop a fatal lymphoproliferative disorder. The cellular mechanism(s) responsible for this phenotype have not been determined. Here, we show that there is a preferential expansion of CD4+ T cells in CTLA-4(-/-) mice, which results in a skewing of the CD4/CD8 T cell ratio. In vivo antibody depletion of CD8+ T cells from birth does not alter the onset or the severity of the CD28-dependent lymphoproliferative disorder. In contrast, CD4+ T cell depletion completely prevents all features characteristic of the lymphoproliferation observed in CTLA-4-deficient mice. These results demonstrate that CD4+ T cells initiate the phenotype in the CTLA-4(-/-) mice. Further, these results suggest that the role of CTLA-4 in peripheral CD4+ versus CD8+ T cell homeostasis is distinct.
CTLA-4缺陷型动物会发展出一种致命的淋巴细胞增生性疾病。导致这种表型的细胞机制尚未确定。在此,我们表明CTLA-4(-/-)小鼠中CD4+ T细胞存在优先扩增,这导致CD4/CD8 T细胞比例失衡。从出生起就在体内用抗体清除CD8+ T细胞,并不会改变CD28依赖性淋巴细胞增生性疾病的发病时间或严重程度。相反,清除CD4+ T细胞则完全阻止了CTLA-4缺陷型小鼠中观察到的淋巴细胞增殖的所有特征。这些结果表明,CD4+ T细胞引发了CTLA-4(-/-)小鼠的表型。此外,这些结果表明CTLA-4在外周CD4+与CD8+ T细胞稳态中的作用是不同的。