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在感染I型单纯疱疹病毒的小鼠脾脏中调节免疫反应的B细胞群体的证明。

Demonstrations of a B-cell population that regulates the immune response in spleens of mice infected with herpes simplex virus type I.

作者信息

Sasaki H, Schmitt D A, Matsumoto K, Pollard R B, Suzuki F

机构信息

Department of Internal Medicine, University of Texas Medical Branch, Galveston 77555-0882.

出版信息

Clin Immunol Immunopathol. 1993 Feb;66(2):169-75. doi: 10.1006/clin.1993.1021.

Abstract

A population of B cells that regulates the immune response was demonstrated in splenic mononuclear cells (SMNC) from mice infected with herpes simplex virus type 1 (HSV). SMNC, obtained from mice 3 days after HSV infection at a dose of 100 LD50, exhibited a reduction in the proliferative response of naive SMNC stimulated with various lectins or allogeneic lymphocytes in a 5-day mixed lymphocyte reaction. Cocultivation of naive SMNC with phagocytic cell-free SMNC (M phi-MNC) from infected mice resulted in the inhibition of lymphocytic blast transformation stimulated with various lectins. These cells were characterized as nylon-wool adherent cells that were eliminated by treatment with anti-Ig antiserum, but not anti-Thy 1.2 monoclonal antibody or anti-asialo GM1 antiserum, followed by complement treatment. In addition, the suppressor cell activity was not demonstrated in M phi-MNC obtained from HSV-infected CBA/CaHN-xid/J mice, which contain a congenital B-cell deficiency. These results suggest that, in addition to suppressor T cells, a population of B cells, which can inhibit lymphocyte proliferations upon stimulation with lectins and alloantigens, might be generated in spleens of mice following HSV infections.

摘要

在感染1型单纯疱疹病毒(HSV)的小鼠的脾单核细胞(SMNC)中,证实了一群调节免疫反应的B细胞。从感染HSV 3天(剂量为100 LD50)的小鼠获得的SMNC,在5天的混合淋巴细胞反应中,对用各种凝集素或同种异体淋巴细胞刺激的未活化SMNC的增殖反应有所降低。将未活化的SMNC与来自感染小鼠的无吞噬细胞的SMNC(M phi-MNC)共培养,导致用各种凝集素刺激的淋巴细胞母细胞转化受到抑制。这些细胞被鉴定为尼龙毛粘附细胞,用抗Ig抗血清处理可将其消除,但用抗Thy 1.2单克隆抗体或抗唾液酸GM1抗血清处理并继以补体处理则不能消除。此外,从感染HSV的CBA/CaHN-xid/J小鼠(其存在先天性B细胞缺陷)获得的M phi-MNC中未显示出抑制细胞活性。这些结果表明,除抑制性T细胞外,在HSV感染后的小鼠脾脏中可能会产生一群B细胞,它们在用凝集素和同种异体抗原刺激后可抑制淋巴细胞增殖。

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