Moorhead J W, Walters C S, Claman H N
J Exp Med. 1973 Feb 1;137(2):411-23. doi: 10.1084/jem.137.2.411.
Both thymus-derived (T) and bone marrow-derived (B) lymphocytes participate in the response to a hapten 4-hydroxy-3-iodo-5-nitrophenylacetic acid (NIP), coupled to a nonimmunogenic isologous carrier, mouse gamma globulin (MGG). Spleen cells from mice immunized with NIP-MGG show increased DNA synthesis in vitro when cultured with NIP-MGG. The participation of and requirement for T cells in the response was demonstrated by treating the spleen cells with anti-theta serum. This treatment resulted in a 77% inhibition of the antigen response. Furthermore, adoptively transferred normal thymus cells could be specifically "activated" by NIP-MGG in vivo and they responded secondarily to the antigen in vitro. The active participation of B cells in the secondary response was demonstrated by passing the immune spleen cells through a column coated with polyvalent anti-MGG serum. Column filtration reduced the number of NIP-specific plaque-forming cells and NIP-specific rosette-forming cells (both functions of B cells) and produced a 47% inhibition of the NIP-MGG response. The ability of the cells to respond to phytohemagglutinin (PHA) was not affected by column filtration showing that T cells were not being selectively removed. The participation of B cells in the in vitro NIP-MGG response was also shown by treatment of the spleen cells with antiserum specific for MGG and MGG determinants. B cells were removed by treatment with anti-IgM or polyvalent anti-MGG serum plus complement, resulting in a respective 46 and 49% inhibition of the response to NIP-MGG. (Treatment with anti-IgM serum had no effect on T cells.) The contribution of the hapten NIP to stimulation of T cells was investigated using NIP-MGG-activated thymus cells. These activated T cells responded in vitro very well to the NIP-MGG complex but not to the MGG carrier alone demonstrating the requirement of the hapten for T cell stimulation. The response was also partially inhibited (41%) by incubating the activated cells with NIP coupled to a single amino acid (epsilon-aminocaproic acid) before addition of NIP-MGG. These results demonstrated that T cells recognize the hapten NIP when it is coupled to the isologous carrier MGG.
胸腺来源的（T）淋巴细胞和骨髓来源的（B）淋巴细胞均参与对半抗原4-羟基-3-碘-5-硝基苯乙酸（NIP）的反应，该半抗原与非免疫原性的同种载体小鼠γ球蛋白（MGG）偶联。用NIP-MGG免疫的小鼠的脾细胞在与NIP-MGG一起培养时，体外DNA合成增加。用抗θ血清处理脾细胞，证明了T细胞在该反应中的参与和需求。这种处理导致抗原反应受到77%的抑制。此外，过继转移的正常胸腺细胞在体内可被NIP-MGG特异性“激活”，并且它们在体外对该抗原产生二次反应。通过使免疫脾细胞通过涂有多价抗MGG血清的柱，证明了B细胞在二次反应中的积极参与。柱过滤减少了NIP特异性噬斑形成细胞和NIP特异性玫瑰花结形成细胞的数量（两者均为B细胞的功能），并对NIP-MGG反应产生了47%的抑制。细胞对植物血凝素（PHA）的反应能力不受柱过滤的影响，表明T细胞未被选择性去除。用对MGG和MGG决定簇特异的抗血清处理脾细胞，也表明了B细胞参与体外NIP-MGG反应。用抗IgM或多价抗MGG血清加补体处理可去除B细胞，分别导致对NIP-MGG反应的46%和49%的抑制。（用抗IgM血清处理对T细胞无影响。）使用NIP-MGG激活的胸腺细胞研究了半抗原NIP对T细胞刺激的作用。这些激活的T细胞在体外对NIP-MGG复合物反应良好，但对单独的MGG载体无反应，这证明了半抗原对T细胞刺激的需求。在加入NIP-MGG之前，用与单个氨基酸（ε-氨基己酸）偶联的NIP孵育激活的细胞，反应也受到部分抑制（41%）。这些结果证明，当半抗原NIP与同种载体MGG偶联时，T细胞能够识别它。
