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

在体内用马红细胞(HRBC)和类脂A(而不是单独用HRBC)诱导的高纯度T细胞在体外可以在没有巨噬细胞的情况下对HRBC或抗α-βT细胞受体(TCR)抗体产生反应。并对无巨噬细胞的细胞增殖机制进行了探讨。从腹膜渗出液细胞(PEC)中提取纯化的T细胞，用[~(3 H)]-胸腺嘧啶核苷(TdR)掺入培养的T细胞对HRBC或抗α-βTCR抗体的反应性进行检测。经HRBC和脂质A刺激的小鼠肺内皮细胞的T细胞[T(HRBC+脂质A)]对这些刺激物的增殖呈剂量依赖性增加，而经HRBC刺激的PEC小鼠的T细胞[T(HRBC)]对这些刺激剂的反应很弱或不增殖。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)明显不同。CD44配体透明质酸或抗CD44(IgG2a)和抗IgG2a抗体作用于T(HRBC+脂质A)细胞后，T(HRBC+Liped A)的增殖受到抑制。相反，在相同条件下，T(HRBC)的增殖被上调。在包被抗CD28抗体的孔洞中，T(HRBC-I-Liped A)对抗α-βTCR抗体的增殖反应增强。这些结果表明，T(HRBC+Liped A)的增殖不仅受TCR的刺激，而且还受CD44和CD28等其他配体的刺激。经AsGM1抗体或抗CD8O抗体和C处理后，T细胞(HRBC+Liped A)的增殖能力被抑制。提示HrBc和LativeA在小鼠体内可产生记忆T细胞群，这种记忆T细胞群不依赖巨噬细胞而能在刺激其TCR时与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.