Objective: To study the expression of dendritic cells in human renal cell carcinoma and explore the cause, so to reveal the mechanism of escaping immune surveillance in RCC. Methods: The expressions of CD83+DCS, CD1a+...Objective: To study the expression of dendritic cells in human renal cell carcinoma and explore the cause, so to reveal the mechanism of escaping immune surveillance in RCC. Methods: The expressions of CD83+DCS, CD1a+DCS,VEGF and TGF-β1 in tumoral, peritumoral and normal kidney tissues of RCC in 30 cases were detected by immunohistochemistry using streptavidin/peroxidese(SP) Results: CD83+DCS were mainly located in the peritumoral areas; whereas CD1a+DCS、were mainly retained within the cancer nests. The number of CD83+DCS was inversely correlated with the clinical stage(P<0.05); but there were no significant correlations between the number of CD1a+DCS、and the clinical stage(P>0.05). The expressions of CD83+DCS and CD1a+DCS have significant difference between the tumoral, peritumoral and normal kidney tissues(P<0.001). The expression of VEGF and TGF-β1 were significantly lower in samples with highly infiltrating CD83+DCS(P<0.05); Whereas CD1a+DCS were not (P>0.05). Conclusion: DC has the tendency to gathering in tumor, but because of the immunosuppressive cytokins, for example VEGF and TGF-β1, inhibits the maturation of DC, there are less mature TIDCS(CD83+TIDCS) in the tumoral tissues, they are mainly located in the peritumoral areas. This may contribute to the mechanism of escaping immune surveillance in RCC.展开更多
AIM： To investigate the morphological characterization of tumor infiltrating dendritic cells （TIDCs） and tumor infiltrating lymphocytes （TILs） in human rectal cancer. METHODS： Light and electron microscopy as we...AIM： To investigate the morphological characterization of tumor infiltrating dendritic cells （TIDCs） and tumor infiltrating lymphocytes （TILs） in human rectal cancer. METHODS： Light and electron microscopy as well as immunohistochemistry were used to observe the distributive and morphological changes of TIDCs and TILs. RESULTS： TIDCs were mainly located in tumor-surrounding tissue. The number of TIDCs in the earlier stage was higher than that in the later stage （P〈 0.01）. TILs were mainly seen in adjacent tissue of cancers and tumor-surrounding tissue. There were more TILs in the earlier stage than that in the later stage （P〈0.01）. Under electron microscope, TIDCs were irregular in shape and exhibited many dendritic protrusions. It isn＇t obvious that cancer cells perforated the basement membrane and TILs were arranged along the basement membrane in the earlier stage. In the later stage, it is explicit that cancer cells perforated the basement membrane and surrounded by TILs. There were contacts among TIDCs, TILs and tumor cell. One IIDCs contacted one or several TILs which clustered around TIDCs. Glycogen granules were seen between TIDCs and Tits. CONCLUSION： The number of TIDCs and TILs is related with tumor progression There exist close relationships among TIDCs, TILs and tumor cell.展开更多
Tumor immunity proceeds through multiple processes, which consist of antigen presentation by antigen presenting cells(APCs) to educate effector cells and destruction by the effector cytotoxic cells. However, tumor imm...Tumor immunity proceeds through multiple processes, which consist of antigen presentation by antigen presenting cells(APCs) to educate effector cells and destruction by the effector cytotoxic cells. However, tumor immunity is frequently repressed at tumor sites. Malignantly transformed cells rarely survive the attack by the immune system, but cells that do survive change their phenotypes to reduce their immunogenicity. The resultant cells evade the attack by the immune system and form clinically discernible tumors. Tumor microenvironments simultaneously contain a wide variety of immune suppressive molecules and cells to dampen tumor immunity. Moreover, the liver microenvironment exhibits immune tolerance to reduce aberrant immune responses to massively-exposed antigens via the portal vein, and immune dysfunction is frequently associated with liver cirrhosis, which is widespread in hepatocellular carcinoma(HCC) patients. Immune therapy aims to reduce tumor burden, but it is also expected to prevent non-cancerous liver lesions from progressing to HCC, because HCC develops or recurs from noncancerous liver lesions with chronic inflammatory states and/or cirrhosis and these lesions cannot be cured and/or eradicated by local and/or systemic therapies. Nevertheless, cancer immune therapy should augment specific tumor immunity by using two distinct measures: enhancing the effector cell functions such as antigen presentation capacity of APCs and tumor cell killing capacity of cytotoxic cells, and reactivating the immune system in immune-suppressive tumor microenvironments. Here, we will summarize the current status and discuss the future perspective on immune therapy for HCC.展开更多
目的探讨子宫内膜癌浸润性树突状细胞(TIDC)凋亡及其凋亡相关蛋白Fas/FasL的表达意义。方法利用S-100单克隆抗体和DNA缺口末端标记(TUNEL法)相结合,分析45例子宫内膜癌组织中TIDC凋亡状况;通过免疫组织化学双重染色方法检测TIDC表面Fas/...目的探讨子宫内膜癌浸润性树突状细胞(TIDC)凋亡及其凋亡相关蛋白Fas/FasL的表达意义。方法利用S-100单克隆抗体和DNA缺口末端标记(TUNEL法)相结合,分析45例子宫内膜癌组织中TIDC凋亡状况;通过免疫组织化学双重染色方法检测TIDC表面Fas/FasL分子表达。结果子宫内膜癌组织中TIDC凋亡发生率显著高于子宫内膜组织中树突状细胞凋亡发生率[(13.02±0.64)%vs(6.82±0.53)%,P<0.05];子宫内膜癌组织TIDC膜表面Fas表达显著低于正常子宫内膜组织(7.88±1.05 vs 19.25±3.03,P<0.05),子宫内膜癌组织TIDC膜表面FasL表达显著高于正常子宫内膜组织(12.95±2.25 vs 7.51±1.14,P<0.05)。结论子宫内膜癌组织中TIDC凋亡增加及Fas、FasL在TIDC上表达失衡,可能导致子宫内膜癌免疫逃逸发生。展开更多
文摘Objective: To study the expression of dendritic cells in human renal cell carcinoma and explore the cause, so to reveal the mechanism of escaping immune surveillance in RCC. Methods: The expressions of CD83+DCS, CD1a+DCS,VEGF and TGF-β1 in tumoral, peritumoral and normal kidney tissues of RCC in 30 cases were detected by immunohistochemistry using streptavidin/peroxidese(SP) Results: CD83+DCS were mainly located in the peritumoral areas; whereas CD1a+DCS、were mainly retained within the cancer nests. The number of CD83+DCS was inversely correlated with the clinical stage(P<0.05); but there were no significant correlations between the number of CD1a+DCS、and the clinical stage(P>0.05). The expressions of CD83+DCS and CD1a+DCS have significant difference between the tumoral, peritumoral and normal kidney tissues(P<0.001). The expression of VEGF and TGF-β1 were significantly lower in samples with highly infiltrating CD83+DCS(P<0.05); Whereas CD1a+DCS were not (P>0.05). Conclusion: DC has the tendency to gathering in tumor, but because of the immunosuppressive cytokins, for example VEGF and TGF-β1, inhibits the maturation of DC, there are less mature TIDCS(CD83+TIDCS) in the tumoral tissues, they are mainly located in the peritumoral areas. This may contribute to the mechanism of escaping immune surveillance in RCC.
基金Supported by Natural Science Foundation of Heilongjiang Province, No.D0234
文摘AIM： To investigate the morphological characterization of tumor infiltrating dendritic cells （TIDCs） and tumor infiltrating lymphocytes （TILs） in human rectal cancer. METHODS： Light and electron microscopy as well as immunohistochemistry were used to observe the distributive and morphological changes of TIDCs and TILs. RESULTS： TIDCs were mainly located in tumor-surrounding tissue. The number of TIDCs in the earlier stage was higher than that in the later stage （P〈 0.01）. TILs were mainly seen in adjacent tissue of cancers and tumor-surrounding tissue. There were more TILs in the earlier stage than that in the later stage （P〈0.01）. Under electron microscope, TIDCs were irregular in shape and exhibited many dendritic protrusions. It isn＇t obvious that cancer cells perforated the basement membrane and TILs were arranged along the basement membrane in the earlier stage. In the later stage, it is explicit that cancer cells perforated the basement membrane and surrounded by TILs. There were contacts among TIDCs, TILs and tumor cell. One IIDCs contacted one or several TILs which clustered around TIDCs. Glycogen granules were seen between TIDCs and Tits. CONCLUSION： The number of TIDCs and TILs is related with tumor progression There exist close relationships among TIDCs, TILs and tumor cell.
基金Supported by(in part)Research Programs on the Innovative Development and Application for New Drugs for Hepatitis B(No.17fk0310116h0001) from the Japan Agency for Medical Research and Development(AMED)Extramural Collaborative Research Grant of Cancer Research Institute,Kanazawa University
文摘Tumor immunity proceeds through multiple processes, which consist of antigen presentation by antigen presenting cells(APCs) to educate effector cells and destruction by the effector cytotoxic cells. However, tumor immunity is frequently repressed at tumor sites. Malignantly transformed cells rarely survive the attack by the immune system, but cells that do survive change their phenotypes to reduce their immunogenicity. The resultant cells evade the attack by the immune system and form clinically discernible tumors. Tumor microenvironments simultaneously contain a wide variety of immune suppressive molecules and cells to dampen tumor immunity. Moreover, the liver microenvironment exhibits immune tolerance to reduce aberrant immune responses to massively-exposed antigens via the portal vein, and immune dysfunction is frequently associated with liver cirrhosis, which is widespread in hepatocellular carcinoma(HCC) patients. Immune therapy aims to reduce tumor burden, but it is also expected to prevent non-cancerous liver lesions from progressing to HCC, because HCC develops or recurs from noncancerous liver lesions with chronic inflammatory states and/or cirrhosis and these lesions cannot be cured and/or eradicated by local and/or systemic therapies. Nevertheless, cancer immune therapy should augment specific tumor immunity by using two distinct measures: enhancing the effector cell functions such as antigen presentation capacity of APCs and tumor cell killing capacity of cytotoxic cells, and reactivating the immune system in immune-suppressive tumor microenvironments. Here, we will summarize the current status and discuss the future perspective on immune therapy for HCC.
文摘目的探讨子宫内膜癌浸润性树突状细胞(TIDC)凋亡及其凋亡相关蛋白Fas/FasL的表达意义。方法利用S-100单克隆抗体和DNA缺口末端标记(TUNEL法)相结合,分析45例子宫内膜癌组织中TIDC凋亡状况;通过免疫组织化学双重染色方法检测TIDC表面Fas/FasL分子表达。结果子宫内膜癌组织中TIDC凋亡发生率显著高于子宫内膜组织中树突状细胞凋亡发生率[(13.02±0.64)%vs(6.82±0.53)%,P<0.05];子宫内膜癌组织TIDC膜表面Fas表达显著低于正常子宫内膜组织(7.88±1.05 vs 19.25±3.03,P<0.05),子宫内膜癌组织TIDC膜表面FasL表达显著高于正常子宫内膜组织(12.95±2.25 vs 7.51±1.14,P<0.05)。结论子宫内膜癌组织中TIDC凋亡增加及Fas、FasL在TIDC上表达失衡,可能导致子宫内膜癌免疫逃逸发生。
