A NONCOGNATE INTERACTION WITH ANTI-RECEPTOR ANTIBODY-ACTIVATED HELPER T-CELLS INDUCES SMALL RESTING MURINE B-CELLS TO PROLIFERATE AND TO SECRETE ANTIBODY
A NONCOGNATE INTERACTION WITH ANTI-RECEPTOR ANTIBODY-ACTIVATED HELPER T-CELLS INDUCES SMALL RESTING MURINE B-CELLS TO PROLIFERATE AND TO SECRETE ANTIBODY
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DOI：
10.1002/eji.1830180312
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发表时间：
1988-03-01
影响因子：
5.4
通讯作者：
OWENS, T
中科院分区：
文献类型：
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作者：
OWENS, T
用两个被F23.1抗T细胞受体抗体激活的T辅助细胞克隆（Th）培养静止的小同种异体B细胞（不相关的单倍型），导致B细胞增殖和分泌抗体的激活。细胞上清液本身对静息B细胞无影响（即使存在完整的F23.1抗体），但可以诱导抗igg预激活的B细胞分泌抗体。两个F23.1+克隆（E9）。D4和4.35F2)和1个F23.1-克隆（D2.2）能与活化E9的上清液协同作用。D4 T细胞诱导B细胞活化。F23.1的F（ab”）2片段诱导E9。D4对B细胞的激活效率与完整的F23.1相同，用F23.1孵育的B细胞群体在用E9培养时没有被激活。D4，虽然T细胞识别细胞呈F23.1，但被弱激活。吸附在塑料上的F23.1的密度降低导致T细胞激活弱，这些T细胞不诱导B细胞反应。半抗原B细胞群，虽然被E9识别。D4，未激活。T细胞和B细胞的分离用0.4-。m膜阻止t依赖性B细胞活化，尽管t细胞衍生的B细胞活化淋巴因子将通过这些膜进行检测。这些结果表明，多克隆非同源B细胞激活依赖于B细胞和活化T细胞之间的物理接触。因此，通过用高密度的T细胞受体配体激活Th细胞，可以克服Th细胞与B细胞同源相互作用以产生和传递B帮助的要求。
Culture of small resting allogeneic B cells (of an irrelevant haplotype) with two clones of T helper (Th) cells that were activated by the F23.1 anti-T cell receptor antibody led to the activation of B cells to proliferate and to secrete antibody. Th cell supernatants by themselves had no effect on resting B cells (even in the presence of intact F23.1 antibody), but could induce antibody secretion by anti-Ig-preactivated B cells. Both F23.1+ clones (E9.D4 and 4.35F2) and one F23.1- clone (D2.2) could synergize with supernatants from activated E9.D4 T cells to induce B cell activation. F(ab'')2 fragments of F23.1 induced E9.D4 to activate B cells as efficienty as intact F23.1, and B cell populations that had been incubated with F23.1 were not activated when cultured with E9.D4, although T cells recognized cell-presented F23.1 and were weakly activated. Reduction of the density of F23.1 adsorbed to plastic resulted in weak T cell activation, and these T cells did not induced B cell responses. Haptenated B cell populations, although recognized by E9.D4, were not activated. Separation of T and B cells by a 0.4-.mu.m membrane prevented T-dependent B cell activation, although Th cell-derived B cell-activating lymphokines would be assayed across these membranes. These results suggest a polyclonal noncognate B cell activation that depends on physical contact between B cells and activated T cells. The requirement for a cognate interaction of Th with B cells for the production and delivery of B help can therefore be overcome by activating Th cells with high densities of T cell receptor ligands.