Antigen-specific proliferative response of memory T cell primed with antigen and bacterial lipopolysaccharide

高度纯化的小鼠T细胞在体内注入马红细胞（HRBC）和脂质A，而不是单独注入HRBC，可以在体外对HRBC或抗α - T细胞受体（TCR）抗体产生增殖反应，而不需要巨噬细胞。探讨无巨噬细胞增殖的机制。从腹膜渗出细胞（PEC）中获得纯化的T细胞，并通过将[^3H]-胸腺嘧啶（TdR）掺入培养的T细胞以对HRBC或抗α - TCR抗体的反应来评估细胞增殖。用HRBC和脂质A刺激小鼠的PEC制备的T细胞[T(HRBC+脂质A)]的增殖对这些刺激物呈剂量依赖性增加，但用HRBC刺激的PEC小鼠制备的T细胞[T(HRBC)]对它们的反应很少或没有增殖。记忆细胞标志物CD44在T（HRBC+脂质a）细胞表面的表达模式与T（HRBC）细胞表面的表达模式明显不同。当细胞在透明质酸（CD44的配体）包被的孔中培养或在先前用抗CD44 （IgG2a）和抗IgG2a抗体处理后培养时，T（HRBC+脂质A）的增殖受到抑制。相反，在相同条件下，T（HRBC）的增殖水平上调。在抗cd28抗体包被的孔中，T（hrbc -i-脂质A）对抗α - TCR抗体的增殖反应增强。这些发现表明，T（HRBC+脂质A）的增殖不仅受到TCR刺激的支持，还受到CD44和CD28等配体刺激的调节。当细胞被AsGM1抗体或抗cd80抗体和c预处理时，T（HRBC+脂质A）的增殖被消除。这些发现表明，HRBC和脂质A在小鼠体内启动时产生记忆T细胞群，当刺激它们的TCR时，它们能够在没有巨噬细胞的帮助下增殖，而是在NK细胞的帮助下增殖。

Highly purified T cells of mice that have been primed in vivo with horse red blood cells (HRBC) and lipid A, but not with HRBC alone, can proliferate in vitro in response to HRBC or anti-alphabeta T cell receptor (TCR) antibody without macrophages. Mechanism of the proliferation without macrophages was investigated. Purified T cells were obtained from the peritoneal exudate cells (PEC) and the cell proliferation was assessed by [^3H]-thymidine (TdR) incorporation into the cultured T cells in response to HRBC or anti-alphabeta TCR antibody. The proliferation of T cells [T(HRBC+lipid A)] that had been prepared from the PEC of the mice primed with HRBC and lipid A increased dose-dependently to these stimulants, but T cells [T(HRBC)] prepared from PEC mice primed with HRBC showed little or no proliferation in response to them. The expression pattern of a memory cell marker, CD44, on the cell surface of T(HRBC+lipid A) was obviously different from that on T(HRBC). The proliferation of T(HRBC+lipid A) was suppressed when the cells were cultured in the wells coated with hyaluronate, a ligand for CD44, or cultured after a previous treatment with anti-CD44 (IgG2a) and anti-IgG2a antibodies. In contrast, the proliferation of T(HRBC) was up-regulated in culture under the same condition. Proliferative responses of T(HRBC-i-lipid A) to anti-alphabeta TCR antibody were enhanced in the wells coated with anti-CD28 antibody. These findings indicate that the proliferation of T(HRBC+lipid A) was riot only supported by a stimulation of TCR but also regulated by the other stimulation via ligand such as for CD44 and CD28. The proliferation of T(HRBC+lipid A) was abolished when the cells had been pretreated with AsGM1 antibody or anti-CD8O antibody and C.These findings indicate that the in vivo priming of mice with HRBC and lipid A generates the memory T cell population that is capable of proliferating without help of macrophages, but with NK cells, when stimulated their TCR.