A water-soluble adjuvant named QuickAntibody （QA） was introduced into the procedure of mouse immunization for the development of hapten-specific monoclonal antibodies （mAbs）, using four kinds of pesticides as mode...A water-soluble adjuvant named QuickAntibody （QA） was introduced into the procedure of mouse immunization for the development of hapten-specific monoclonal antibodies （mAbs）, using four kinds of pesticides as model compounds. Compared with conventional Freund＇s adjuvants, QA treatments offered relatively low but acceptable antiserum titers after three inoculations, gave little adverse effects to the experimental animals, and were preferable in harvesting splenocytes during the steps of cell fusion. Afterwards, hybridomas from the QA group were prepared and screened by both non-competitive and competitive indirect enzyme-linked immunosorbent assays （ELISAs）. The efficiency of gaining immune-positive hybridomas was satisfactory, and the resultant mAbs showed sensitivities （half maximal inhibitory concentration （IC50）） of 0.91, 2.46, 3.72, and 6.22 ng/ml to triazophos, parathion, chlorpyrifos, and fenpropathrin, respectively. Additionally, the performance of QA adjuvant was further confirmed by acquiring a high-affinity mAb against okadaic acid （IC50 of 0.36 ng/ml） after three immunizations. These newly developed mAbs showed similar or even better sensitivities compared with previously reported mAbs specific to the corresponding analytes. This study suggested that the easy-to-use adjuvant could be applicable to the efficient gen- eration of highly sensitive mAbs against small compounds.展开更多
Objective The aim of this study was to costimulate the CD3-AK cells with anti-CD28 monoclonal antibody (mAb), observe the effect of cell proliferation and cytotoxicity and explore the regulatory role of CD28 mAb on t...Objective The aim of this study was to costimulate the CD3-AK cells with anti-CD28 monoclonal antibody (mAb), observe the effect of cell proliferation and cytotoxicity and explore the regulatory role of CD28 mAb on the CD3-AK tumoricidal activity.展开更多
CD3-specific monoclonal antibody was the first one used for clinical practice in field of transplantation. Recently, renewed interests have elicited in its capacity to prevent autoimmune diabetes by inducing immune to...CD3-specific monoclonal antibody was the first one used for clinical practice in field of transplantation. Recently, renewed interests have elicited in its capacity to prevent autoimmune diabetes by inducing immune tolerance. In this study, we tested whether this antibody can also be used to treat another kind of autoimmune disease myasthenia gravis （MG） and explored the possible mechanisms. MG is caused by an autoimmune damage mediated by antibody- and complement-mediated destruction of AChR at the neuromuscular junction. We found that administration of CD3-specific antibody （Fab）2 to an animal model with experimental autoimmune myasthenia gravis （EAMG） （B6 mice received 3 times of AChR/CFA immunization） could not significantly improve the clinical signs and clinical score. When the possible mechanisms were tested, we found that CD3 antibody treatment slightly down-regulated the T-cell response to AChR, modestly up-regulation the muscle strength. And no significant difference in the titers of IgG2b was found between CD3 antibody treated and control groups. These data indicated that CD3-specific antibody was not suitable for treating MG, an antibody- and complementmediated autoimmune disease, after this disease has been established. The role of CD3-specific antibody in treating this kind of disease remains to be determined. Cellular ＆ Molecular Immunology. 2005;2（6）：461-465.展开更多
基金supported by the Special Fund for Agro-scientific Research in the Public Interest(No.201203094-3)the Scientific Research Fund of Zhejiang Provincial Education Department(No.Y201329970)+1 种基金the National Natural Science Foundation of China(No.31401768)the Experimental Technology Research Project of Zhejiang University(No.SZD201404),China
文摘A water-soluble adjuvant named QuickAntibody （QA） was introduced into the procedure of mouse immunization for the development of hapten-specific monoclonal antibodies （mAbs）, using four kinds of pesticides as model compounds. Compared with conventional Freund＇s adjuvants, QA treatments offered relatively low but acceptable antiserum titers after three inoculations, gave little adverse effects to the experimental animals, and were preferable in harvesting splenocytes during the steps of cell fusion. Afterwards, hybridomas from the QA group were prepared and screened by both non-competitive and competitive indirect enzyme-linked immunosorbent assays （ELISAs）. The efficiency of gaining immune-positive hybridomas was satisfactory, and the resultant mAbs showed sensitivities （half maximal inhibitory concentration （IC50）） of 0.91, 2.46, 3.72, and 6.22 ng/ml to triazophos, parathion, chlorpyrifos, and fenpropathrin, respectively. Additionally, the performance of QA adjuvant was further confirmed by acquiring a high-affinity mAb against okadaic acid （IC50 of 0.36 ng/ml） after three immunizations. These newly developed mAbs showed similar or even better sensitivities compared with previously reported mAbs specific to the corresponding analytes. This study suggested that the easy-to-use adjuvant could be applicable to the efficient gen- eration of highly sensitive mAbs against small compounds.
文摘Objective The aim of this study was to costimulate the CD3-AK cells with anti-CD28 monoclonal antibody (mAb), observe the effect of cell proliferation and cytotoxicity and explore the regulatory role of CD28 mAb on the CD3-AK tumoricidal activity.
文摘CD3-specific monoclonal antibody was the first one used for clinical practice in field of transplantation. Recently, renewed interests have elicited in its capacity to prevent autoimmune diabetes by inducing immune tolerance. In this study, we tested whether this antibody can also be used to treat another kind of autoimmune disease myasthenia gravis （MG） and explored the possible mechanisms. MG is caused by an autoimmune damage mediated by antibody- and complement-mediated destruction of AChR at the neuromuscular junction. We found that administration of CD3-specific antibody （Fab）2 to an animal model with experimental autoimmune myasthenia gravis （EAMG） （B6 mice received 3 times of AChR/CFA immunization） could not significantly improve the clinical signs and clinical score. When the possible mechanisms were tested, we found that CD3 antibody treatment slightly down-regulated the T-cell response to AChR, modestly up-regulation the muscle strength. And no significant difference in the titers of IgG2b was found between CD3 antibody treated and control groups. These data indicated that CD3-specific antibody was not suitable for treating MG, an antibody- and complementmediated autoimmune disease, after this disease has been established. The role of CD3-specific antibody in treating this kind of disease remains to be determined. Cellular ＆ Molecular Immunology. 2005;2（6）：461-465.
