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

已经在体内用马红细胞（HRBC）和脂质A（但不是单独用HRBC）致敏的小鼠的高度纯化的T细胞可以在体外响应于HRBC或抗α T细胞受体（TCR）抗体而增殖，而不需要巨噬细胞。探讨了无巨噬细胞的增殖机制。从腹膜渗出液细胞（PEC）中获得纯化的T细胞，并通过[^3H]-胸苷（TdR）掺入培养的T细胞中以响应HRBC或抗α TCR抗体来评估细胞增殖。从HRBC和脂质A致敏的小鼠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，但从HRBC致敏的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CD 44在T细胞表面的表达模式与T细胞表面的表达模式明显不同。当细胞在涂有透明质酸盐（CD 44的配体）的威尔斯孔中培养时，或在用抗CD 44（IgG 2a）和抗IgG 2a抗体预先处理后培养时，T（HRBC+脂质A）的增殖受到抑制。相反，T（HRBC）的增殖在相同条件下的培养中上调。在用抗-CD 28抗体包被的威尔斯孔中，T（HRBC-1-lipid A）对抗-α TCR抗体的应答增强。这些发现表明T（HRBC+lipid A）的增殖不仅受到TCR刺激的支持，而且还受到通过配体如CD 44和CD 28的其他刺激的调节。当细胞已经用AsGM 1抗体或抗CD 8 O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，用HRBC和脂质A对小鼠进行体内引发产生记忆T细胞群，该记忆T细胞群能够在没有巨噬细胞的帮助下增殖，但在刺激其TCR时用NK细胞增殖。

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.