Nakane A, Okamoto M, Asano M, Kohanawa M, Minagawa T
Department of Microbiology, Hokkaido University School of Medicine, Sapporo, Japan.
Infect Immun. 1993 Jul;61(7):2786-92. doi: 10.1128/iai.61.7.2786-2792.1993.
Mice were protected against a lethal infection with Listeria monocytogenes when treated with low doses of an anti-CD3 monoclonal antibody (MAb). Injection of anti-CD3 MAb induced rapid production of endogenous tumor necrosis factor (TNF) in the spleens and endogenous gamma interferon (IFN-gamma) in the bloodstreams and spleens of mice. Administration of anti-Thy1.2 MAb or a combination of anti-CD4 MAb and anti-CD8 MAb resulted in suppression of anti-CD3 MAb-induced endogenous cytokine production and antilisterial resistance. Alternatively, in vivo depletion of anti-CD3 MAb-induced TNF and IFN-gamma by the simultaneous administration of antibodies against TNF and IFN-gamma suppressed anti-CD3 MAb-induced antilisterial resistance. Moreover, injection of anti-complement receptor type 3 (Mac-1, CD11b) resulted in inhibition of anti-CD3 MAb-induced antilisterial resistance. These results suggest that the preventive effect of anti-CD3 MAb might be due to activation of phagocytes by TNF and IFN-gamma induced by stimulating CD4+ T cells and CD8+ T cells with the MAb. Furthermore, treatment with anti-CD3 MAb did not inhibit establishment of acquired resistance against secondary infection with L. monocytogenes.
用低剂量抗CD3单克隆抗体（MAb）治疗时，小鼠对单核细胞增生李斯特菌的致死性感染具有抵抗力。注射抗CD3 MAb可诱导小鼠脾脏中内源性肿瘤坏死因子（TNF）快速产生，并在小鼠血流和脾脏中诱导内源性γ干扰素（IFN-γ）产生。给予抗Thy1.2 MAb或抗CD4 MAb与抗CD8 MAb的组合会导致抗CD3 MAb诱导的内源性细胞因子产生和抗李斯特菌抗性受到抑制。另外，通过同时给予抗TNF和抗IFN-γ抗体在体内消耗抗CD3 MAb诱导的TNF和IFN-γ，会抑制抗CD3 MAb诱导的抗李斯特菌抗性。此外，注射抗补体受体3（Mac-1，CD11b）会抑制抗CD3 MAb诱导的抗李斯特菌抗性。这些结果表明，抗CD3 MAb的预防作用可能是由于用该MAb刺激CD4 + T细胞和CD8 + T细胞诱导的TNF和IFN-γ激活了吞噬细胞。此外，用抗CD3 MAb治疗不会抑制对单核细胞增生李斯特菌继发感染的获得性抗性的建立。
