Iwamoto I, Tomoe S, Tomioka H, Takatsu K, Yoshida S
Second Department of Internal Medicine, Chiba University School of Medicine, Japan.
J Leukoc Biol. 1992 Nov;52(5):572-8. doi: 10.1002/jlb.52.5.572.
Previous studies suggested that the eosinophil recruitment into the site of cutaneous late-phase reaction (LPR) was dependent on IgE antibody and mast cells. In this study, we determined the role of CD4+ T cells and CD8+ T cells in causing antigen-induced eosinophil recruitment of LPR in mouse skin. Eosinophil infiltration into the subcutaneous tissue of ovalbumin (OVA)-sensitized BALB/c mice was biphasic, reaching the first peak at 6 h after the subcutaneous challenge with OVA and the second peak at 24 to 48 h. The in vivo depletion of CD4+ T cells by pretreatment with anti-L3T4 monoclonal antibody (mAb) significantly decreased the second peak (at 24 h and 48 h), but not the first peak (at 6 h), of OVA-induced eosinophil infiltration into the skin of OVA-sensitized mice. However, the depletion of CD8+ T cells by pretreatment with anti-Lyt-2 mAb had no significant effect on either the first peak or second peak of OVA-induced cutaneous eosinophilia. Pretreatment with anti-murine interleukin-5 (IL-5) mAb also decreased the second peak, but not the first peak, of OVA-induced cutaneous eosinophilia. In contrast to the inhibitory effects of depletion of CD4+ T cells and of anti-IL-5 mAb on the second peak of antigen-induced cutaneous eosinophilia, disodium cromoglycate and a selective antagonist for platelet activating factor (PAF) CV-6209 decreased the first peak of OVA-induced cutaneous eosinophilia in the mouse. These results indicate that CD4+ T cells, but not CD8+ T cells, cause the second peak of antigen-induced eosinophil recruitment of cutaneous LPR and that IL-5 mediates this eosinophil recruitment. In contrast, the first peak of antigen-induced eosinophil recruitment of cutaneous LPR is mediated by mast cells and PAF.
先前的研究表明，嗜酸性粒细胞募集到皮肤迟发相反应（LPR）部位依赖于IgE抗体和肥大细胞。在本研究中，我们确定了CD4⁺ T细胞和CD8⁺ T细胞在引起小鼠皮肤抗原诱导的LPR嗜酸性粒细胞募集中的作用。卵清蛋白（OVA）致敏的BALB/c小鼠皮下组织中的嗜酸性粒细胞浸润是双相的，在皮下注射OVA后6小时达到第一个峰值，在24至48小时达到第二个峰值。用抗L3T4单克隆抗体（mAb）预处理在体内耗竭CD4⁺ T细胞，可显著降低OVA诱导的嗜酸性粒细胞浸润到OVA致敏小鼠皮肤中的第二个峰值（在24小时和48小时），但不影响第一个峰值（在6小时）。然而，用抗Lyt-2 mAb预处理耗竭CD8⁺ T细胞，对OVA诱导的皮肤嗜酸性粒细胞增多的第一个峰值或第二个峰值均无显著影响。用抗小鼠白细胞介素-5（IL-5）mAb预处理也降低了OVA诱导的皮肤嗜酸性粒细胞增多的第二个峰值，但不影响第一个峰值。与耗竭CD4⁺ T细胞和抗IL-5 mAb对抗原诱导的皮肤嗜酸性粒细胞增多第二个峰值的抑制作用相反，色甘酸钠和血小板活化因子（PAF）的选择性拮抗剂CV-6209降低了小鼠中OVA诱导皮肤嗜酸性粒细胞增多的第一个峰值。这些结果表明，CD4⁺ T细胞而非CD8⁺ T细胞引起皮肤LPR抗原诱导的嗜酸性粒细胞募集的第二个峰值，且IL-5介导这种嗜酸性粒细胞募集。相比之下，皮肤LPR抗原诱导的嗜酸性粒细胞募集的第一个峰值由肥大细胞和PAF介导。
