Patel M, Havas H F
Immunology. 1982 May;46(1):97-105.
In order to analyse the mechanism of immunosuppression of plasmacytoma-bearing mice, the role of enriched T cells, B cells, and adherent cells from the spleens of normal and TEPC-183 plasmacytoma (IgM,k) bearing mice in the primary immune response was investigated. Nylon-wool-enriched fractions of T and B cells were used in the study of T-cell-dependent immune responses to the 2-4-6-trinitrophenyl ligand. When 5 × 10 M 2-mercaptoethanol (2-ME) was present in cultures, TEPC-183 spleen cells or their T- or B-cell-enriched fractions did not suppress the immune responses of normal spleen cells. However, in the absence of 2-ME, T- or B-cell fractions were as effective as unfractionated TEPC-183 spleen cells in causing suppression of normal immune responses. T and B cells derived from TEPC-183 spleens gave minimal anti-trinitrophenyl specific plaque-forming-cell responses when co-cultured with adherent cells from either normal or TEPC-183 spleens. In contrast, either T- or B-cell fractions from TEPC-183 spleens were at least partially competent when co-cultured with B or T cells from normal spleens. The data thus suggest that the suppressed state of TEPC-183 spleen cells may be due to defective T—B cell interaction. It was consistently observed that splenic adherent cells from TEPC-183-bearing mice were neither suppressed nor suppressive for the immune responses of normal splenic lymphocytes at the ratios tested. Adherent peritoneal exudate (PE) cells from either normal or TEPC-183-bearing mice were equally suppressive for the immune responses of normal splenic lymphocytes at the PE cell to lymphocyte ratios of 1:10 and 1:35. Thus, the suppressive characteristic of adherent PE cells in this system is not specific for TEPC-183 plasmacytoma in mice. TEPC-183 spleens were found to contain 35% or more esterase-positive cells, compared with approximately 5% esterase-positive cells present in normal spleens. The possible role of esterase-positive cells, T cells, B cells, and adherent cells in the observed suppression will be discussed.
为了分析荷浆细胞瘤小鼠免疫抑制的机制,研究了来自正常小鼠和荷TEPC - 183浆细胞瘤(IgM,κ)小鼠脾脏中富集的T细胞、B细胞和贴壁细胞在初次免疫应答中的作用。T细胞和B细胞的尼龙毛富集组分用于研究对2,4,6 - 三硝基苯基配体的T细胞依赖性免疫应答。当培养物中存在5×10 M 2 - 巯基乙醇(2 - ME)时,TEPC - 183脾细胞或其T细胞或B细胞富集组分不会抑制正常脾细胞的免疫应答。然而,在不存在2 - ME的情况下,T细胞或B细胞组分在抑制正常免疫应答方面与未分级的TEPC - 183脾细胞一样有效。当与来自正常或TEPC - 183脾脏的贴壁细胞共培养时,源自TEPC - 183脾脏的T细胞和B细胞产生的抗三硝基苯基特异性空斑形成细胞应答最小。相反,当与来自正常脾脏的B细胞或T细胞共培养时,TEPC - 183脾脏的T细胞或B细胞组分至少部分具有功能。因此,数据表明TEPC - 183脾细胞的抑制状态可能是由于T - B细胞相互作用缺陷。一直观察到,在测试的比例下,来自荷TEPC - 183小鼠的脾脏贴壁细胞对正常脾淋巴细胞的免疫应答既没有被抑制也没有抑制作用。来自正常或荷TEPC - 183小鼠的贴壁腹腔渗出液(PE)细胞在PE细胞与淋巴细胞比例为1:10和1:35时,对正常脾淋巴细胞的免疫应答具有同样的抑制作用。因此,该系统中贴壁PE细胞的抑制特性并非小鼠中TEPC - 183浆细胞瘤所特有的。发现TEPC - 183脾脏含有35%或更多的酯酶阳性细胞,而正常脾脏中约有5%的酯酶阳性细胞。将讨论酯酶阳性细胞、T细胞、B细胞和贴壁细胞在观察到的抑制作用中的可能作用。