ABSTRACT
@#[摘 要] 恶性肿瘤是严重威胁人类生命的疾病之一，近年来免疫治疗已经成为肿瘤治疗的焦点，解决免疫治疗只对部分患者有效的问题迫在眉睫。在肿瘤微环境（tumor microenvironment，TME）中趋化因子介导细胞的定向移动，同时具有多种调节功能，既可以作用于免疫细胞，也可直接作用于肿瘤细胞，发挥了复杂的生物学作用。CXC趋化因子受体3（CXC chemokine receptor 3，CXCR3）通过与其同源CXC趋化因子配体9（CXC chemokine ligand 9，CXCL9）/10/11结合，不仅参与了肿瘤发生、侵袭并促进肿瘤相关血管的形成，同时也介导了免疫细胞向肿瘤组织中浸润，为无免疫反应性或免疫反应性差的“冷肿瘤”转变为免疫反应性的“热肿瘤”提供了新的思路，并且可能成为治疗的新靶点。这种抗肿瘤和促肿瘤的双重作用，似乎与CXCR3变体（CXCR3-A、CXCR3-B）发挥相反的作用密切相关。本文就近年来CXCR3变体CXCR3-A、CXCR3-B及其配体CXCL9/10/11在TME中作用的研究进展展开综述。
ABSTRACT
AIM: To investigate the immunologic mechanism of CXC chemokine ligand 10(CXCL10) and its receptor CXC chemokine receptor 3 (CXCR3 ) involved in the process of endometriosis (EM). METHODS: Serum samples were collected from 3 groups; EM patients without operation (n = 76) , EM patients with operation (n = 10) and the normal control persons (n =76). CXCL10 and CA12S concentrations were detected by means of ELISA and chemilumino-metry. Cell surface antigens on the activated PBMC - CD3 and CXCR3, as well as CXCR3 subgene - CXCR3A and CX-CR3B were tested by flow cytometry (FC) and RT - PCR when PBMC was separated from women with EM ( n = 10) and without EM (n = 10), and then activated. RESULTS: Serum CXCL10 concentrations between three groups were signifi-canly different (P < 0.05). Compared to normal control group, although the supernatant CXCL10 concentration and CD3~+ /CXCR3~+ PBMC number in EM group has no significant difference (P >0.05) , highly expressed CXCR3B in EM group rather than CXCR3A was observed. CONCLUSION: CXCL10 in women with EM is low, indicating that it plays a vital role in the process of EM and immune system of the women with EM is defected and impaired. The immunoreactivity of PBMC from both EM patients and normal person is same to activated signal, but the productions are different: PBMC in EM group mainly express CXCR3B but PBMC in normal person mainly express CXCR3A after activation, which may be one of the immune mechanisms that EM escapes from immunological lethal effect of the infected host.