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Volume 4,Issue 1,1997 Table of Contents
1 The Effects of Integrins CD11/CD18 on the Binding Capacities Between Human Monocytes and Tumor Cells
1997, 4(1):5-9.
DOI: 10.3872/j.issn.1007-385X.1997.1.002
Abstract:
本文报道用无毒性的活体荧光染料—钙黄绿素 AM标记的肿瘤细胞与人单核细胞共培养4小时,用Cyto Fluo 2300测定细胞粘附能力的荧光检测技术.结果表明IFN-γ和LPS激活的人单核细胞能迅速地与悬浮生长的人肿瘤细胞、B淋巴母细胞及淋巴细胞粘附.激活的人单核细胞表达更多的CD11a、CD11b、CD11c和CD18,对肿瘤细胞有更多的粘附性.抗体封闭及蛋白激酶抑制物处理细胞,粘附能力均受到明显的抑制.IFN-γ和LPS处理肿瘤细胞也能明显增加两种细胞间的粘附能力.上述结果提示人单核细胞粘附能力的增加与整合素及肿瘤细胞所表达的相关配体增加有关.
本文报道用无毒性的活体荧光染料—钙黄绿素 AM标记的肿瘤细胞与人单核细胞共培养4小时,用Cyto Fluo 2300测定细胞粘附能力的荧光检测技术.结果表明IFN-γ和LPS激活的人单核细胞能迅速地与悬浮生长的人肿瘤细胞、B淋巴母细胞及淋巴细胞粘附.激活的人单核细胞表达更多的CD11a、CD11b、CD11c和CD18,对肿瘤细胞有更多的粘附性.抗体封闭及蛋白激酶抑制物处理细胞,粘附能力均受到明显的抑制.IFN-γ和LPS处理肿瘤细胞也能明显增加两种细胞间的粘附能力.上述结果提示人单核细胞粘附能力的增加与整合素及肿瘤细胞所表达的相关配体增加有关.
1997, 4(1):10-13.
DOI: 10.3872/j.issn.1007-385X.1997.1.003
Abstract:
In this study, we demonstrated that immobilized fibronectin (FN) enhanced LAK activity, and that the enhanced LAK activity was completely abrogated by an anti-VLA-5 monoclonal antibody and RGD peptide. Fresh -spleen cells expressed VLA-4, VLA-6 and vitronectin receptor, whereas VLA-5 was expressed only on the spleen cells activated with IL-2. LAK cells showed increased adhesion to immobilized FN compared with that to control BSA, and the increased adhesion of LAK cells to immobilized FN was inhibited by anti-VLA-5 monoclonal antibody. Conjugate-formation assay showed that the LAK cells cultured on immobilized FN bound to target cells more efficiently than the control LAK cells, and that anti-LFA-1 monoclonal antibody inhibited the LAK-target cell binding. Immobilized type IV collagen and laminin, as well as FN, enhanced LAK activity. All these results suggest that the interaction of inte-grins expressed on LAK cells with extracellular matrix proteins act as co-stimulator for the enhancement of LAK activity , and that anchorage is necessary for full activation of LAK cells.
In this study, we demonstrated that immobilized fibronectin (FN) enhanced LAK activity, and that the enhanced LAK activity was completely abrogated by an anti-VLA-5 monoclonal antibody and RGD peptide. Fresh -spleen cells expressed VLA-4, VLA-6 and vitronectin receptor, whereas VLA-5 was expressed only on the spleen cells activated with IL-2. LAK cells showed increased adhesion to immobilized FN compared with that to control BSA, and the increased adhesion of LAK cells to immobilized FN was inhibited by anti-VLA-5 monoclonal antibody. Conjugate-formation assay showed that the LAK cells cultured on immobilized FN bound to target cells more efficiently than the control LAK cells, and that anti-LFA-1 monoclonal antibody inhibited the LAK-target cell binding. Immobilized type IV collagen and laminin, as well as FN, enhanced LAK activity. All these results suggest that the interaction of inte-grins expressed on LAK cells with extracellular matrix proteins act as co-stimulator for the enhancement of LAK activity , and that anchorage is necessary for full activation of LAK cells.
1997, 4(1):14-19.
DOI: 10.3872/j.issn.1007-385X.1997.1.004
Abstract:
We have studied the effects of B7-1 on antitumor immunity induced in vivo by murine B7-1 gene transfected EL-4 lymphoma. At a lethal dose of wild - type(wt) or plasmid controlled (pc) B7-1 negative tumor cells. B7-1 gone transfected EL-4 cells inoculated in syngeneic mice were regressed. In contrast to the mice immunized with B7-1 tumor cells, immunization of mice with B7-l~EL-4 tumor cells showed significant protective effects against the sequence rechallenge of wt EL-4 tumor. Vaccination with X-irradiated B7-1 positive tumor cells at the early stage ( 7 days) after inoculation of wt EL-4 tumor cells showed some therapeutically effects but not at the late stage (14 days after inoculation). Vaccination with B7-l~ EL-4 tumor cells delayed the occurrence of wt EL-4 tumors and prolonged the survival period of tumor-bearing mice. Our results indicate that the transfcction of B7-1 into tumor cells can increase the immunogenicity of EL-4 tumor and improve host response to wt EL-4 lymphoma. Immunization with B7-1 positive tumors can elicit effective antitumor immunity.
We have studied the effects of B7-1 on antitumor immunity induced in vivo by murine B7-1 gene transfected EL-4 lymphoma. At a lethal dose of wild - type(wt) or plasmid controlled (pc) B7-1 negative tumor cells. B7-1 gone transfected EL-4 cells inoculated in syngeneic mice were regressed. In contrast to the mice immunized with B7-1 tumor cells, immunization of mice with B7-l~EL-4 tumor cells showed significant protective effects against the sequence rechallenge of wt EL-4 tumor. Vaccination with X-irradiated B7-1 positive tumor cells at the early stage ( 7 days) after inoculation of wt EL-4 tumor cells showed some therapeutically effects but not at the late stage (14 days after inoculation). Vaccination with B7-l~ EL-4 tumor cells delayed the occurrence of wt EL-4 tumors and prolonged the survival period of tumor-bearing mice. Our results indicate that the transfcction of B7-1 into tumor cells can increase the immunogenicity of EL-4 tumor and improve host response to wt EL-4 lymphoma. Immunization with B7-1 positive tumors can elicit effective antitumor immunity.
1997, 4(1):20-25.
DOI: 10.3872/j.issn.1007-385X.1997.1.005
Abstract:
A crucial role in eliciting anti-tumor immunity of costimulatory molecule CD80(B7-1) has been demonstrated by animal experimental studies.In this paper, CD80 expression in human tumor cell lines and EBV-transformed B cell was detected using RT-PCR and FACS methods. The results showed that CD80 expression of Raji and EBV-transformed B cell was positive but that of 3AO,MCF-7,MDA-453,MKN-45, Hela was negative. We have constructed retroviral vector CD80-pLN,transfected package cell PA317, screened high titer rctrovirus supernatant then infected human tumor cell lines and gained CD80 positive tumor cell clones. With pre-and post-CD80-transfected human breast carcinoma cell line MDA-453,the upregulated expression of ICAM-I, HLA class I molecule was observed, but the expression of HLA class II molecule wasn't changed.
A crucial role in eliciting anti-tumor immunity of costimulatory molecule CD80(B7-1) has been demonstrated by animal experimental studies.In this paper, CD80 expression in human tumor cell lines and EBV-transformed B cell was detected using RT-PCR and FACS methods. The results showed that CD80 expression of Raji and EBV-transformed B cell was positive but that of 3AO,MCF-7,MDA-453,MKN-45, Hela was negative. We have constructed retroviral vector CD80-pLN,transfected package cell PA317, screened high titer rctrovirus supernatant then infected human tumor cell lines and gained CD80 positive tumor cell clones. With pre-and post-CD80-transfected human breast carcinoma cell line MDA-453,the upregulated expression of ICAM-I, HLA class I molecule was observed, but the expression of HLA class II molecule wasn't changed.
Yong-Qing Li
,
Masanobu Kobayashi
,
Yasuhiro Kuramitsu
,
Lan Yuan
,
Kazuhi-ro Matsushita
,
Hideo Yagita
,
Ko Okumura
,
Masuo Hosokawa
1997, 4(1):26-34.
DOI: 10.3872/j.issn.1007-385X.1997.1.006
Abstract:
In this study, we demonstrated that immobilized fibronectin (FN) enhanced LAK activity, and that the enhanced LAK activity was completely abrogated by an anti-VLA-5 monoclonal antibody and RGD peptide. Fresh -spleen cells expressed VLA-4, VLA-6 and vitronectin receptor, whereas VLA-5 was expressed only on the spleen cells activated with IL-2. LAK cells showed increased adhesion to immobilized FN compared with that to control BSA, and the increased adhesion of LAK cells to immobilized FN was inhibited by anti-VLA-5 monoclonal antibody. Conjugate-formation assay showed that the LAK cells cultured on immobilized FN bound to target cells more efficiently than the control LAK cells, and that anti-LFA-1 monoclonal antibody inhibited the LAK-target cell binding. Immobilized type IV collagen and laminin, as well as FN, enhanced LAK activity. All these results suggest that the interaction of inte-grins expressed on LAK cells with extracellular matrix proteins act as co-stimulator for the enhancement of LAK activity , and that anchorage is necessary for full activation of LAK cells.
In this study, we demonstrated that immobilized fibronectin (FN) enhanced LAK activity, and that the enhanced LAK activity was completely abrogated by an anti-VLA-5 monoclonal antibody and RGD peptide. Fresh -spleen cells expressed VLA-4, VLA-6 and vitronectin receptor, whereas VLA-5 was expressed only on the spleen cells activated with IL-2. LAK cells showed increased adhesion to immobilized FN compared with that to control BSA, and the increased adhesion of LAK cells to immobilized FN was inhibited by anti-VLA-5 monoclonal antibody. Conjugate-formation assay showed that the LAK cells cultured on immobilized FN bound to target cells more efficiently than the control LAK cells, and that anti-LFA-1 monoclonal antibody inhibited the LAK-target cell binding. Immobilized type IV collagen and laminin, as well as FN, enhanced LAK activity. All these results suggest that the interaction of inte-grins expressed on LAK cells with extracellular matrix proteins act as co-stimulator for the enhancement of LAK activity , and that anchorage is necessary for full activation of LAK cells.
1997, 4(1):35-38.
DOI: 10.3872/j.issn.1007-385X.1997.1.007
Abstract:
In the present study, the expression of MHC class I molecule and ICAM - 1 on the surface of B16 melanoma cells were observed, and their roles in the induction of CTL were investigated. The results showed that both MHC class I and ICAM - 1 expression increased after IL-2, IL-4, or IL-6 gene transfection. The splenocyte CTL activity was enhanced significantly after in vivo immunization with cytokine gene - transfected B16 melanoma cells. The CTL induction was partly inhibited by anti-ICAM-1 mAb and was completely abolished by anti-MHC class I mAb. These results suggested the increased immunogenicity of IL-2,IL-4 or IL-6 gene-transfected B16 melanoma cells may be related to the upregula-tion of ICAM-1 or MHC class I molecules after cytokine gene transfection.
In the present study, the expression of MHC class I molecule and ICAM - 1 on the surface of B16 melanoma cells were observed, and their roles in the induction of CTL were investigated. The results showed that both MHC class I and ICAM - 1 expression increased after IL-2, IL-4, or IL-6 gene transfection. The splenocyte CTL activity was enhanced significantly after in vivo immunization with cytokine gene - transfected B16 melanoma cells. The CTL induction was partly inhibited by anti-ICAM-1 mAb and was completely abolished by anti-MHC class I mAb. These results suggested the increased immunogenicity of IL-2,IL-4 or IL-6 gene-transfected B16 melanoma cells may be related to the upregula-tion of ICAM-1 or MHC class I molecules after cytokine gene transfection.
1997, 4(1):39-42.
DOI: 10.3872/j.issn.1007-385X.1997.1.008
Abstract:
血管细胞粘附分子一1(VCAM-1)是一种属于免疫球蛋白超家族成员的细胞粘附分子,其配体主要是整合素家族的α4β1/VLA一4(非常晚出现抗原一4).近年来发现VCAM一1亦在巨噬细胞、树突状细胞上有表达,但目前对其在这些专职抗原递呈细胞上表达的性质和作用尚不完全明确.本研究通过流式细胞仪(FACS发现VCAM一1是组成性地表达在巨噬细胞上,并且其表达可在抗原、TNF-a作用后上调;在混合淋巴细胞反应中发现VCAM-1/VLA-4在巨噬细胞活化T细胞中具有较强的刺激作用,抗VCAM一1和抗VIA一4单抗的阻断能降低混合培养上清中IL-2的表达水平.这些结果提示VCAM—1的表达不仅有助于巨噬细胞与其它细胞的粘附接触,而且在通过VLA-4共刺激活化T细胞中也起重要作用.
血管细胞粘附分子一1(VCAM-1)是一种属于免疫球蛋白超家族成员的细胞粘附分子,其配体主要是整合素家族的α4β1/VLA一4(非常晚出现抗原一4).近年来发现VCAM一1亦在巨噬细胞、树突状细胞上有表达,但目前对其在这些专职抗原递呈细胞上表达的性质和作用尚不完全明确.本研究通过流式细胞仪(FACS发现VCAM一1是组成性地表达在巨噬细胞上,并且其表达可在抗原、TNF-a作用后上调;在混合淋巴细胞反应中发现VCAM-1/VLA-4在巨噬细胞活化T细胞中具有较强的刺激作用,抗VCAM一1和抗VIA一4单抗的阻断能降低混合培养上清中IL-2的表达水平.这些结果提示VCAM—1的表达不仅有助于巨噬细胞与其它细胞的粘附接触,而且在通过VLA-4共刺激活化T细胞中也起重要作用.
1997, 4(1):43-46.
DOI: 10.3872/j.issn.1007-385X.1997.1.009
Abstract:
为了探讨人TNF-α基因修饰的成纤维细胞在体内的抗肿瘤作用,本文应用含脑心肌炎病毒(EMCV)内核糖体进入位点(IRES)的双顺反子逆转录病毒载体pGCEN/TNF-α来转导TNF-α基因至小鼠成纤维细胞NIH3T3.人TNF-α基因修饰的成纤维细胞NIH3T3/TNF-α能持续高水平表达TNF-α,在小鼠肝癌H22细胞皮下植入后第3天或第7天,肿瘤部位直接注射2.5×10~5NIH3T3/TNF-α.或1×10~6NIH3T3/TNF-α能明显抑制肿瘤生长(P<0.05),增加小鼠存活率(P<0.025).可见人INF-α基因修饰的成纤维细胞有望成为一种安全、简便且有效的肿瘤生物治疗新途径
为了探讨人TNF-α基因修饰的成纤维细胞在体内的抗肿瘤作用,本文应用含脑心肌炎病毒(EMCV)内核糖体进入位点(IRES)的双顺反子逆转录病毒载体pGCEN/TNF-α来转导TNF-α基因至小鼠成纤维细胞NIH3T3.人TNF-α基因修饰的成纤维细胞NIH3T3/TNF-α能持续高水平表达TNF-α,在小鼠肝癌H22细胞皮下植入后第3天或第7天,肿瘤部位直接注射2.5×10~5NIH3T3/TNF-α.或1×10~6NIH3T3/TNF-α能明显抑制肿瘤生长(P<0.05),增加小鼠存活率(P<0.025).可见人INF-α基因修饰的成纤维细胞有望成为一种安全、简便且有效的肿瘤生物治疗新途径
1997, 4(1):47-50.
DOI: 10.3872/j.issn.1007-385X.1997.1.010
Abstract:
本工作以逆转录病毒为载体将TNF-α基因导入胃癌细胞系MKN28和BGC823,经筛选获阳性克隆MKN28-TNF和BCC823-TNF.对TNF基因在肿瘤细胞中的表达及其对肿瘤细胞的作用进行了探讨.证明外源TNF基因在肿瘤细胞中获得表达;肿瘤细胞生长速度明显减慢,生长抑制率分别达71%和 66%.HTdR掺入率在TNF基因转染细胞明显降低.转染后的肿瘤细胞丧失了裸鼠体内成瘤能力.实验结果表明TNF基因导入胃癌细胞后,细胞生长及致癌能力受到明显抑制,为TNF最终能用于临床胃癌基因治疗提供了有意义的资料.
本工作以逆转录病毒为载体将TNF-α基因导入胃癌细胞系MKN28和BGC823,经筛选获阳性克隆MKN28-TNF和BCC823-TNF.对TNF基因在肿瘤细胞中的表达及其对肿瘤细胞的作用进行了探讨.证明外源TNF基因在肿瘤细胞中获得表达;肿瘤细胞生长速度明显减慢,生长抑制率分别达71%和 66%.HTdR掺入率在TNF基因转染细胞明显降低.转染后的肿瘤细胞丧失了裸鼠体内成瘤能力.实验结果表明TNF基因导入胃癌细胞后,细胞生长及致癌能力受到明显抑制,为TNF最终能用于临床胃癌基因治疗提供了有意义的资料.
1997, 4(1):54-57.
DOI: 10.3872/j.issn.1007-385X.1997.1.012
Abstract:
The immunosuppressive effect of supernatant of the cultured tumor cells, including breast adenocarcinoma ( MCF-7, MDA-453 ), gastrocarcinoma ( MKN-45 ), cervical cancer ( Hela ) and ovarian cancer ( 3AO ), was studied by MTT assay. The results showed that the supernatant of tumor cell culture suppressed the proliferation of lymphocytes activated with PHA. The supernatant of cultured tumor cells, except that of cultured MDA-453 cells, also suppressed the cytotoxic activity of LAK cells. It is suggested that there are immunosuppressive factors in the supernatant of tumor cell culture. But the immunosuppressive effect of supernatant derived from the cultured tumor cells treated with sodium phenylacetate that is a noncytotoxic differentiation inducer on the proliferation of lymphocytes activated with PHA and the cytotoxic activity of LAK cells , was decreased significantly. It indicates that sodium phenylacetate could decrease the immunosuppressive factors derived from tumor cells.
The immunosuppressive effect of supernatant of the cultured tumor cells, including breast adenocarcinoma ( MCF-7, MDA-453 ), gastrocarcinoma ( MKN-45 ), cervical cancer ( Hela ) and ovarian cancer ( 3AO ), was studied by MTT assay. The results showed that the supernatant of tumor cell culture suppressed the proliferation of lymphocytes activated with PHA. The supernatant of cultured tumor cells, except that of cultured MDA-453 cells, also suppressed the cytotoxic activity of LAK cells. It is suggested that there are immunosuppressive factors in the supernatant of tumor cell culture. But the immunosuppressive effect of supernatant derived from the cultured tumor cells treated with sodium phenylacetate that is a noncytotoxic differentiation inducer on the proliferation of lymphocytes activated with PHA and the cytotoxic activity of LAK cells , was decreased significantly. It indicates that sodium phenylacetate could decrease the immunosuppressive factors derived from tumor cells.
1997, 4(1):61-63.
DOI: 10.3872/j.issn.1007-385X.1997.1.014
Abstract:
We have studied the effects of B7-1 on antitumor immunity induced in vivo by murine B7-1 gene transfected EL-4 lymphoma. At a lethal dose of wild - type(wt) or plasmid controlled (pc) B7-1 negative tumor cells. B7-1 gone transfected EL-4 cells inoculated in syngeneic mice were regressed. In contrast to the mice immunized with B7-1 tumor cells, immunization of mice with B7-l~EL-4 tumor cells showed significant protective effects against the sequence rechallenge of wt EL-4 tumor. Vaccination with X-irradiated B7-1 positive tumor cells at the early stage ( 7 days) after inoculation of wt EL-4 tumor cells showed some therapeutically effects but not at the late stage (14 days after inoculation). Vaccination with B7-l~ EL-4 tumor cells delayed the occurrence of wt EL-4 tumors and prolonged the survival period of tumor-bearing mice. Our results indicate that the transfcction of B7-1 into tumor cells can increase the immunogenicity of EL-4 tumor and improve host response to wt EL-4 lymphoma. Immunization with B7-1 positive tumors can elicit effective antitumor immunity.
We have studied the effects of B7-1 on antitumor immunity induced in vivo by murine B7-1 gene transfected EL-4 lymphoma. At a lethal dose of wild - type(wt) or plasmid controlled (pc) B7-1 negative tumor cells. B7-1 gone transfected EL-4 cells inoculated in syngeneic mice were regressed. In contrast to the mice immunized with B7-1 tumor cells, immunization of mice with B7-l~EL-4 tumor cells showed significant protective effects against the sequence rechallenge of wt EL-4 tumor. Vaccination with X-irradiated B7-1 positive tumor cells at the early stage ( 7 days) after inoculation of wt EL-4 tumor cells showed some therapeutically effects but not at the late stage (14 days after inoculation). Vaccination with B7-l~ EL-4 tumor cells delayed the occurrence of wt EL-4 tumors and prolonged the survival period of tumor-bearing mice. Our results indicate that the transfcction of B7-1 into tumor cells can increase the immunogenicity of EL-4 tumor and improve host response to wt EL-4 lymphoma. Immunization with B7-1 positive tumors can elicit effective antitumor immunity.
1997, 4(1):64-67.
DOI: 10.3872/j.issn.1007-385X.1997.1.015
Abstract:
In this experiment, we introduced human interleukin-2(lL-2)gene and Neomycin resistance (Neo~R) gene into a human lung adenocarcinoma cell line GLC, using a retroviral vector PLXSN. The positive cells obtained by selecting in G418 were compared with the wild-type cells. We observed their growth characteristics in vitro and the quantity of IL-2 in the culture supernatants. PCR result demonstrated the integration of foreign genes into tumor genome DNA after transfection and permanent existence. Under electron microscope, what can be seen was the surface villi of trans-duced-cells are less and shorter. It deserves further investigation to determine whether the change of cell surface influence metastatic ability of cells.
In this experiment, we introduced human interleukin-2(lL-2)gene and Neomycin resistance (Neo~R) gene into a human lung adenocarcinoma cell line GLC, using a retroviral vector PLXSN. The positive cells obtained by selecting in G418 were compared with the wild-type cells. We observed their growth characteristics in vitro and the quantity of IL-2 in the culture supernatants. PCR result demonstrated the integration of foreign genes into tumor genome DNA after transfection and permanent existence. Under electron microscope, what can be seen was the surface villi of trans-duced-cells are less and shorter. It deserves further investigation to determine whether the change of cell surface influence metastatic ability of cells.
1997, 4(1):68-70.
DOI: 10.3872/j.issn.1007-385X.1997.1.016
Abstract:
A crucial role in eliciting anti-tumor immunity of costimulatory molecule CD80(B7-1) has been demonstrated by animal experimental studies.In this paper, CD80 expression in human tumor cell lines and EBV-transformed B cell was detected using RT-PCR and FACS methods. The results showed that CD80 expression of Raji and EBV-transformed B cell was positive but that of 3AO,MCF-7,MDA-453,MKN-45, Hela was negative. We have constructed retroviral vector CD80-pLN,transfected package cell PA317, screened high titer rctrovirus supernatant then infected human tumor cell lines and gained CD80 positive tumor cell clones. With pre-and post-CD80-transfected human breast carcinoma cell line MDA-453,the upregulated expression of ICAM-I, HLA class I molecule was observed, but the expression of HLA class II molecule wasn't changed.
A crucial role in eliciting anti-tumor immunity of costimulatory molecule CD80(B7-1) has been demonstrated by animal experimental studies.In this paper, CD80 expression in human tumor cell lines and EBV-transformed B cell was detected using RT-PCR and FACS methods. The results showed that CD80 expression of Raji and EBV-transformed B cell was positive but that of 3AO,MCF-7,MDA-453,MKN-45, Hela was negative. We have constructed retroviral vector CD80-pLN,transfected package cell PA317, screened high titer rctrovirus supernatant then infected human tumor cell lines and gained CD80 positive tumor cell clones. With pre-and post-CD80-transfected human breast carcinoma cell line MDA-453,the upregulated expression of ICAM-I, HLA class I molecule was observed, but the expression of HLA class II molecule wasn't changed.
1997, 4(1):75-77.
DOI: 10.3872/j.issn.1007-385X.1997.1.019
Abstract:
血管细胞粘附分子一1(VCAM-1)是一种属于免疫球蛋白超家族成员的细胞粘附分子,其配体主要是整合素家族的α4β1/VLA一4(非常晚出现抗原一4).近年来发现VCAM一1亦在巨噬细胞、树突状细胞上有表达,但目前对其在这些专职抗原递呈细胞上表达的性质和作用尚不完全明确.本研究通过流式细胞仪(FACS发现VCAM一1是组成性地表达在巨噬细胞上,并且其表达可在抗原、TNF-a作用后上调;在混合淋巴细胞反应中发现VCAM-1/VLA-4在巨噬细胞活化T细胞中具有较强的刺激作用,抗VCAM一1和抗VIA一4单抗的阻断能降低混合培养上清中IL-2的表达水平.这些结果提示VCAM—1的表达不仅有助于巨噬细胞与其它细胞的粘附接触,而且在通过VLA-4共刺激活化T细胞中也起重要作用.
血管细胞粘附分子一1(VCAM-1)是一种属于免疫球蛋白超家族成员的细胞粘附分子,其配体主要是整合素家族的α4β1/VLA一4(非常晚出现抗原一4).近年来发现VCAM一1亦在巨噬细胞、树突状细胞上有表达,但目前对其在这些专职抗原递呈细胞上表达的性质和作用尚不完全明确.本研究通过流式细胞仪(FACS发现VCAM一1是组成性地表达在巨噬细胞上,并且其表达可在抗原、TNF-a作用后上调;在混合淋巴细胞反应中发现VCAM-1/VLA-4在巨噬细胞活化T细胞中具有较强的刺激作用,抗VCAM一1和抗VIA一4单抗的阻断能降低混合培养上清中IL-2的表达水平.这些结果提示VCAM—1的表达不仅有助于巨噬细胞与其它细胞的粘附接触,而且在通过VLA-4共刺激活化T细胞中也起重要作用.
联系方式
- 《中国肿瘤生物治疗杂志》
- 1994年创刊
- 主办单位：Chinese Society of Immunology, Chinese Anti-cancer Association
- 邮编：200433
- 电话：021-81871002-22
- 电子邮箱：cjcb@biother.cn
- 网址:http://www.biother.cn
- 刊号：ISSN 1007-385X
- CN 31-1725/R
- 国内定价： ￥20元/册
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.
Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.