Yetter R A, Buller R M, Lee J S, Elkins K L, Mosier D E, Fredrickson T N, Morse H C
Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892.
J Exp Med. 1988 Aug 1;168(2):623-35. doi: 10.1084/jem.168.2.623.
Mice depleted in vivo of CD4+ Th cells by treatment with mAb GK1.5 were found to be resistant to the lymphoproliferative/immunodeficiency disease (MAIDS) induced in intact mice by infection with the mixture of LP-BM5 murine leukemia viruses. Depleted mice did not develop lymphadenopathy or splenomegaly, had normal serum IgM levels, normal CTL responses to alloantigens, and were able to generate PFC responses to Th-independent antigens even though frequencies of virus-producing spleen cells were comparable in depleted and intact mice. Depletion of CD4+ Th cells after infection resulted in a reversal of many abnormalities exhibited by infected controls; spleen weights, serum IgM levels, and allogeneic CTL responses of treated mice were comparable to those of uninfected controls. These results demonstrate that dysfunction of CD4+ Th cells is central to the induction and progression of both T and B cell abnormalities in MAIDS.
通过用单克隆抗体GK1.5处理在体内耗尽CD4 + Th细胞的小鼠,发现其对由LP - BM5鼠白血病病毒混合物感染完整小鼠诱导的淋巴细胞增殖/免疫缺陷疾病(MAIDS)具有抗性。耗尽CD4 + Th细胞的小鼠未出现淋巴结病或脾肿大,血清IgM水平正常,对同种异体抗原的CTL反应正常,并且即使在耗尽CD4 + Th细胞的小鼠和完整小鼠中产生病毒的脾细胞频率相当,它们也能够对非Th依赖性抗原产生PFC反应。感染后耗尽CD4 + Th细胞导致感染对照组出现的许多异常情况发生逆转;处理过的小鼠的脾脏重量、血清IgM水平和同种异体CTL反应与未感染对照组相当。这些结果表明,CD4 + Th细胞功能障碍是MAIDS中T和B细胞异常诱导和进展的核心。