Iwamoto I, Nakajima H, Endo H, Yoshida S
Second Department of Internal Medicine, Chiba University School of Medicine, Japan.
J Exp Med. 1993 Feb 1;177(2):573-6. doi: 10.1084/jem.177.2.573.
We have previously shown that antigen-induced eosinophil recruitment into the tissue of sensitized mice is mediated by CD4+ T cells and interleukin 5. To determine whether interferon gamma (IFN-gamma) regulates antigen-induced eosinophil recruitment into the tissue, we studied the effect of recombinant (r) murine IFN-gamma and of anti-IFN-gamma monoclonal antibody (mAb) on the eosinophil infiltration of the trachea induced by antigen inhalation in mice. The intraperitoneal administration of rIFN-gamma prevented antigen-induced eosinophil infiltration in the trachea of sensitized mice. The administration of rIFN-gamma also decreased antigen-induced CD4+ T cell but not CD8+ T cell infiltration in the trachea. On the other hand, pretreatment with anti-IFN-gamma mAb enhanced antigen-induced eosinophil and CD4+ T cell infiltration in the trachea. These results indicate that IFN-gamma regulates antigen-induced eosinophil recruitment into the tissue by inhibiting CD4+ T cell infiltration.
我们之前已经表明，抗原诱导的嗜酸性粒细胞募集到致敏小鼠的组织中是由CD4 + T细胞和白细胞介素5介导的。为了确定干扰素γ（IFN-γ）是否调节抗原诱导的嗜酸性粒细胞募集到组织中，我们研究了重组（r）小鼠IFN-γ和抗IFN-γ单克隆抗体（mAb）对小鼠吸入抗原诱导的气管嗜酸性粒细胞浸润的影响。腹腔注射rIFN-γ可防止抗原诱导的致敏小鼠气管嗜酸性粒细胞浸润。rIFN-γ的给药也减少了抗原诱导的气管中CD4 + T细胞的浸润，但没有减少CD8 + T细胞的浸润。另一方面，用抗IFN-γ mAb预处理可增强抗原诱导的气管嗜酸性粒细胞和CD4 + T细胞浸润。这些结果表明，IFN-γ通过抑制CD4 + T细胞浸润来调节抗原诱导的嗜酸性粒细胞募集到组织中。
