The 8^th International Workshop on Human Leucocyte Differentiation Antigens （chaired by HZ and managed by BS） was run over a 4-year period and culminated in a conference in December 2004. Here we review the achievem...The 8^th International Workshop on Human Leucocyte Differentiation Antigens （chaired by HZ and managed by BS） was run over a 4-year period and culminated in a conference in December 2004. Here we review the achievements of the HLDA Workshops and provide links to information on CD molecules and antibodies against them, including the 93 new CDs assigned in the 8^th Workshop. We consider what remains to be achieved （including an estimate of the number of leucocyte surface molecules still to be discovered）, and how the field can best move forward.展开更多
AIM: To evaluate the role of baicalin in ulcerative colitis (UC) with regard to the CD4<sup>+</sup>CD29<sup>+</sup> T helper cell, its surface markers and serum inflammatory cytokines.
目的分析CD4^+CD29^+T细胞含量及细胞毒性T淋巴细胞相关抗原4(CTLA-4)、程序坏死因子1(PD-1)及程序坏死因子配体1(PD-L1)免疫检查点表达水平与非小细胞肺癌患者的化疗效果及远期存活率的关系。方法选取2015年1月至2017年1月沧州市中心...目的分析CD4^+CD29^+T细胞含量及细胞毒性T淋巴细胞相关抗原4(CTLA-4)、程序坏死因子1(PD-1)及程序坏死因子配体1(PD-L1)免疫检查点表达水平与非小细胞肺癌患者的化疗效果及远期存活率的关系。方法选取2015年1月至2017年1月沧州市中心医院收治的100例非小细胞肺癌患者;采用流式细胞术检测患者血中CD4^+CD29^+T、CTLA-4^+T、PD-1^+T及PD-L1^+T细胞水平;随访2年,记录患者生存情况,分为存活组79例,死亡组21例;依照RECIST Version 1.1标准对患者化疗效果进行评估,并按此分为缓解组54例,进展组46例。比较各组的CD4+CD29+T、CTLA-4^+T、PD-1^+T及PD-L1^+T细胞水平,分析以上各细胞水平与患者疗效及远期存活率之间的相关关系。结果化疗缓解组CD4^+CD29^+T、CTLA-4^+T及PD-1^+T细胞水平均高于进展组[(22.74±1.92)%vs.(18.04±2.15)%、(28.91±1.24)%vs.(20.13±1.77)%、(26.29±1.19)%vs.(18.94±1.64)%],PD-L1+T细胞水平低于进展组[(17.22±1.07)%vs.(22.73±1.25)%],差异均有统计学意义(P<0.05);存活组CD4+CD29+T、CTLA-4+T及PD-1+T细胞水平均高于死亡组[(22.11±1.17)%vs.(14.81±1.64)%、(28.32±1.24)%vs.(11.90±1.93)%、(25.88±2.01)%vs.(11.73±2.06)%],PD-L1+T细胞水平低于死亡组[(16.41±2.72)%vs.(24.81±2.11)%],差异均有统计学意义(P<0.05)。CD4^+CD29^+T、CTLA-4^+T、PD-1^+T细胞水平与患者疗效及远期存活率呈正相关(P<0.05),PD-L1^+T细胞水平与患者疗效及远期存活率呈负相关(P<0.05)。结论非小细胞肺癌患者血中CD4^+CD29^+、CTLA-4^+、PD-1^+T细胞水平与化疗效果及远期生存呈正相关,PD-L1+T细胞水平与其呈负相关关系。展开更多
Background The mechanism of chronic immune activation and impairment of HIV-specific immune responses during chronic infection is not fully understood. However, it is known that high immune activation leads to more ra...Background The mechanism of chronic immune activation and impairment of HIV-specific immune responses during chronic infection is not fully understood. However, it is known that high immune activation leads to more rapid progression to AIDS. We hypothesize that CD4^＋ T cell-mediated viral antigen presentation contributes to this pathologic immune activation in HIV-infected individuals. Methods HIV-specific T cells, responding to noninfectious HIV-1 virions as antigen, were measured by flow cytometric assays. These experimental conditions reflect the in vivo condition where noninfectious HIV-1 represents more than 99% of the antigens. Results CD4^＋ T cells purified from HIV-infected individuals were capable of cross presenting exogenous noninfectious HIV-1 virions to HIV-1-specific CD8^＋ T cells. Cross presentation required the entry of HIV-1 to CD4^＋ T cells and antigen translocation from endoplasmic reticulum to the Golgi complex. Blocking CD4^＋ mediated activation of HIV-specific CD8^＋ T cells and redirecting the viral antigens to antigen presenting cells improved HIV-specific T cell responses. Contusions One possible cause of chronic immune activation and impairment of HIV-1 specific T cell responses is represented by HIV-1 harboring CD4^＋ T cells cross presenting HIV-1 antigen to activate CD8^＋ T cells. This new mechanism provides the first evidence that cross presentation of noninfectious HIV-1 virions play a role in the immunopathogenesis of HIV-1 infection.展开更多
文摘The 8^th International Workshop on Human Leucocyte Differentiation Antigens （chaired by HZ and managed by BS） was run over a 4-year period and culminated in a conference in December 2004. Here we review the achievements of the HLDA Workshops and provide links to information on CD molecules and antibodies against them, including the 93 new CDs assigned in the 8^th Workshop. We consider what remains to be achieved （including an estimate of the number of leucocyte surface molecules still to be discovered）, and how the field can best move forward.
基金Supported by National Natural Science Foundation of Chinunder Grant No.30772701
文摘AIM: To evaluate the role of baicalin in ulcerative colitis (UC) with regard to the CD4<sup>+</sup>CD29<sup>+</sup> T helper cell, its surface markers and serum inflammatory cytokines.
文摘目的分析CD4^+CD29^+T细胞含量及细胞毒性T淋巴细胞相关抗原4(CTLA-4)、程序坏死因子1(PD-1)及程序坏死因子配体1(PD-L1)免疫检查点表达水平与非小细胞肺癌患者的化疗效果及远期存活率的关系。方法选取2015年1月至2017年1月沧州市中心医院收治的100例非小细胞肺癌患者;采用流式细胞术检测患者血中CD4^+CD29^+T、CTLA-4^+T、PD-1^+T及PD-L1^+T细胞水平;随访2年,记录患者生存情况,分为存活组79例,死亡组21例;依照RECIST Version 1.1标准对患者化疗效果进行评估,并按此分为缓解组54例,进展组46例。比较各组的CD4+CD29+T、CTLA-4^+T、PD-1^+T及PD-L1^+T细胞水平,分析以上各细胞水平与患者疗效及远期存活率之间的相关关系。结果化疗缓解组CD4^+CD29^+T、CTLA-4^+T及PD-1^+T细胞水平均高于进展组[(22.74±1.92)%vs.(18.04±2.15)%、(28.91±1.24)%vs.(20.13±1.77)%、(26.29±1.19)%vs.(18.94±1.64)%],PD-L1+T细胞水平低于进展组[(17.22±1.07)%vs.(22.73±1.25)%],差异均有统计学意义(P<0.05);存活组CD4+CD29+T、CTLA-4+T及PD-1+T细胞水平均高于死亡组[(22.11±1.17)%vs.(14.81±1.64)%、(28.32±1.24)%vs.(11.90±1.93)%、(25.88±2.01)%vs.(11.73±2.06)%],PD-L1+T细胞水平低于死亡组[(16.41±2.72)%vs.(24.81±2.11)%],差异均有统计学意义(P<0.05)。CD4^+CD29^+T、CTLA-4^+T、PD-1^+T细胞水平与患者疗效及远期存活率呈正相关(P<0.05),PD-L1^+T细胞水平与患者疗效及远期存活率呈负相关(P<0.05)。结论非小细胞肺癌患者血中CD4^+CD29^+、CTLA-4^+、PD-1^+T细胞水平与化疗效果及远期生存呈正相关,PD-L1+T细胞水平与其呈负相关关系。
基金This study was supported by a grant from the Major Basic Project of China (973) (No. 2005CB522903).
文摘Background The mechanism of chronic immune activation and impairment of HIV-specific immune responses during chronic infection is not fully understood. However, it is known that high immune activation leads to more rapid progression to AIDS. We hypothesize that CD4^＋ T cell-mediated viral antigen presentation contributes to this pathologic immune activation in HIV-infected individuals. Methods HIV-specific T cells, responding to noninfectious HIV-1 virions as antigen, were measured by flow cytometric assays. These experimental conditions reflect the in vivo condition where noninfectious HIV-1 represents more than 99% of the antigens. Results CD4^＋ T cells purified from HIV-infected individuals were capable of cross presenting exogenous noninfectious HIV-1 virions to HIV-1-specific CD8^＋ T cells. Cross presentation required the entry of HIV-1 to CD4^＋ T cells and antigen translocation from endoplasmic reticulum to the Golgi complex. Blocking CD4^＋ mediated activation of HIV-specific CD8^＋ T cells and redirecting the viral antigens to antigen presenting cells improved HIV-specific T cell responses. Contusions One possible cause of chronic immune activation and impairment of HIV-1 specific T cell responses is represented by HIV-1 harboring CD4^＋ T cells cross presenting HIV-1 antigen to activate CD8^＋ T cells. This new mechanism provides the first evidence that cross presentation of noninfectious HIV-1 virions play a role in the immunopathogenesis of HIV-1 infection.
