Nonoyama S, Smith F O, Ochs H D
Department of Pediatrics, University of Washington, Seattle 98195.
J Immunol. 1993 Oct 1;151(7):3894-901.
To explore the extent of immune reconstitution of SCID mice by human peripheral blood lymphocytes (hu-PBL-SCID mice), we studied the production of immunoglobulin isotypes and specific antibody (Ab) by the engrafted human cells. Human IgG was detectable in 94% of hu-PBL-SCID mice. IgE synthesis by hu-PBL-SCID mice correlated with the IgE levels observed in human donors. All SCID mice receiving PBL obtained from human donors previously immunized with the T-cell-dependent Ag, bacteriophage phi x 174 (phage), produced phage neutralizing antibody. Quantity and quality (Ig isotypes) of phage-specific Ab produced by hu-PBL-SCID mice correlated with that observed in the donor serum. Human B cells alone failed to engraft, and T cells were required for the production of Ig and anti-phage Ab. Phage-specific Ab production occurred without direct Ag exposure of the hu-PBL-SCID mice, suggesting that the specific Ab production was induced directly by polyclonal activation of the engrafted human cells. Intravenous phage injections given 4 wk after cell transfer failed to further increase the anti-phage Ab titer. Phage neutralizing Ab production could not be boosted if spleen cells obtained from hu-PBL-SCID mice were cultured in the presence of Ag. However, hu-PBL-SCID mice produced increased amounts of anti-phage Ab, providing they were injected with phage at the time of cell transfer. Injection of phage at the time of cell transfer, but not 4 wk later, to mice receiving PBL from nonimmunized donors induced production of minute amounts of anti-phage Ab. We conclude that human peripheral blood lymphocytes transferred into SCID mice become maximally stimulated presumably by xenogeneic murine Ag, resulting in polyclonal expansion of the graft and spontaneous production of Ab to Ag the human donor was previously exposed to, and in loss of responses to subsequent Ag exposure. Ab production to neoantigen, however, can be induced and that to recall Ag can be modified if PBL are exposed to Ag at the time of cell transfer.
为了探究人外周血淋巴细胞对重症联合免疫缺陷(SCID)小鼠免疫重建的程度(人外周血淋巴细胞 - SCID小鼠),我们研究了植入的人细胞产生免疫球蛋白同种型和特异性抗体(Ab)的情况。在94%的人外周血淋巴细胞 - SCID小鼠中可检测到人类IgG。人外周血淋巴细胞 - SCID小鼠的IgE合成与人供体中观察到的IgE水平相关。所有接受先前用T细胞依赖性抗原噬菌体φx174(噬菌体)免疫的人供体的外周血淋巴细胞的SCID小鼠都产生了噬菌体中和抗体。人外周血淋巴细胞 - SCID小鼠产生的噬菌体特异性抗体的数量和质量(Ig同种型)与供体血清中观察到的情况相关。单独的人B细胞无法植入,产生Ig和抗噬菌体抗体需要T细胞。人外周血淋巴细胞 - SCID小鼠在没有直接接触抗原的情况下产生了噬菌体特异性抗体,这表明特异性抗体的产生是由植入的人细胞的多克隆激活直接诱导的。细胞转移4周后静脉注射噬菌体未能进一步提高抗噬菌体抗体滴度。如果在抗原存在的情况下培养从人外周血淋巴细胞 - SCID小鼠获得的脾细胞,噬菌体中和抗体的产生无法增强。然而,如果在细胞转移时给人外周血淋巴细胞 - SCID小鼠注射噬菌体,它们会产生更多的抗噬菌体抗体。在细胞转移时而非4周后给从未免疫的供体接受外周血淋巴细胞的小鼠注射噬菌体,会诱导产生微量的抗噬菌体抗体。我们得出结论,转移到SCID小鼠中的人外周血淋巴细胞可能受到异种小鼠抗原的最大刺激,导致移植物的多克隆扩增以及对人供体先前接触过的抗原自发产生抗体,并且对随后的抗原接触失去反应。然而,如果外周血淋巴细胞在细胞转移时接触抗原,对新抗原的抗体产生可以被诱导,对回忆抗原的抗体产生可以被改变。