DIFFERENTIAL MACROPHAGE REQUIREMENTS FOR T-HELPER CELL AND T-HELPER CELL-INDUCED LYMPHOCYTE-B PROLIFERATION

DIFFERENTIAL MACROPHAGE REQUIREMENTS FOR T-HELPER CELL AND T-HELPER CELL-INDUCED LYMPHOCYTE-B PROLIFERATION
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DOI:
10.1084/jem.157.1.312
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发表时间:
1983-01-01
影响因子:
15.3
通讯作者:
COUTINHO, A
COUTINHO, A
中科院分区:
医学1区
文献类型:
--
作者:
BANDEIRA, A;POBOR, G;COUTINHO, A

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针对B细胞和巨噬细胞表面表达的次要抗原的主要组织相容性复合体限制性辅助性T细胞克隆,当面对适当的T细胞耗尽的小鼠脾细胞时,被诱导增殖,进而激活靶向应答B细胞,使其多克隆生长和成熟。辅助性细胞群的照射表明,它们的效应功能(和B淋巴细胞反应)与增殖活性无关。Sephadex G10柱上的贴壁细胞耗尽,虽然完全消除了辅助T细胞的增殖,但并不能消除辅助细胞诱导的B细胞反应,这表明巨噬细胞对这两种细胞生长的需求存在显著的数量差异。由于在巨噬细胞极度耗尽的情况下,巨噬细胞与启动的辅助T细胞相互作用时可检测到显著的B细胞反应,因此巨噬细胞在T-B细胞协作中的作用显然仅限于扩增最佳数量的辅助T淋巴细胞。因此,激活的辅助细胞可以自主地产生所有B细胞特异性的生长和成熟因子,介导协同抗体反应。巨噬细胞耗尽后,脂多糖诱导的反应显著减少,这表明在胸腺非依赖性B细胞的生长和/或成熟过程中,辅助细胞产生了这些因子。
Major histocompatibility complex-restricted helper T cell clones against minor antigens expressed on B cell and macrophage surfaces, when confronted with appropriate T cell-depleted mouse spleen cells, are induced to proliferation and, in turn, activate target-responder B cells to polyclonal growth and maturation. Irradiation of helper cell populations demonstrates that their effector functions (and B lymphocyte responses) are independent of proliferative activity. Adherent cell depletion on Sephadex G10 columns, while completely abrogating helper T cell proliferation, does not abolish helper cell-induced B cell responses, demonstrating a remarkable quantitative difference in macrophage requirements for the growth of these 2 cell types. Because significant B cell responses are detected upon interaction with primed helper T cells under conditions of extreme macrophage depletion, the role of macrophages in T-B cell cooperation is apparently limited to expansion of optimal numbers of helper T lymphocytes. It follows that activated helper cells can autonomously produce all B cell-specific growth and maturation factors mediating cooperative antibody responses. The profound reduction of lipopolysaccharide-induced responses upon macrophage depletion suggests accessory cell production of such factors in thymus-independent B cell growth and/or maturation.