The novel coronavirus SARS-CoV-2 has infected more than 104 million individuals and resulted in more than 2.2 million deaths worldwide as of February 7,2021(https://covid19.who.int).The COVID-19 pandemic highlights th...The novel coronavirus SARS-CoV-2 has infected more than 104 million individuals and resulted in more than 2.2 million deaths worldwide as of February 7,2021(https://covid19.who.int).The COVID-19 pandemic highlights the need for safe and effective vaccines against SARS-CoV-2 infection.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 tole...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
Biological agents threats people's life through different ways,one of which lies in the impairment of cognition.It is believed cognitive decline may result from biological agents mediated neuron damage directly,or...Biological agents threats people's life through different ways,one of which lies in the impairment of cognition.It is believed cognitive decline may result from biological agents mediated neuron damage directly,or from the activation of the host immune response to eradicate the pathogen.However,direct linkage between infections and cognitive decline is very limited.Here we focus on the mechanisms of how different biological virus or they induced systemic and local inflammation link to the cognitive impairment,focusing on the roles of acti-vated microglia and several molecular pathways mediated neurotoxicity.展开更多
The complement C5 anaphylatoxin receptor is a member of the seven transmembrane-spanning G protein-coupled receptor superfamily that signals through Gcxi and Gtz16. C5aR is mostly expressed on neutrophils, macrophages...The complement C5 anaphylatoxin receptor is a member of the seven transmembrane-spanning G protein-coupled receptor superfamily that signals through Gcxi and Gtz16. C5aR is mostly expressed on neutrophils, macrophages and endothelial cells. C5a and C5aR interaction plays an important role in numerous biological effects such as in vivo cytokine storm which results in inflammatory damage. Considering the limitation of collection of human peripheral blood neutrophils and their short half life, the stably transfected cell line for studying the biological effects of C5aR is needed. In this study, we transfected C5aR gene into Molt-4 cell line and examined the function of ectopic C5aR. Our results showed stable expression of the C5aR in Molt-4 cell line and their interaction with human C5a induced ERKI/2 phosphorylation, Ca＋＋ influx. This stable transfected cell line may provide a useful tool for studying signal pathways related to C5a and C5aR interplay and antibody development specific for C5aR. Cellular ＆ Molecular Immunology.展开更多
基金supported by the National Key Plan for Scientific Research and Development of China(2020YFC0860100,2020YFC0841401,2016YFD0500306)the National Natural Science Foundation of China(82041006)the National Science and Technology Major Project of China(No.2017ZX10304402003001).
文摘The novel coronavirus SARS-CoV-2 has infected more than 104 million individuals and resulted in more than 2.2 million deaths worldwide as of February 7,2021(https://covid19.who.int).The COVID-19 pandemic highlights the need for safe and effective vaccines against SARS-CoV-2 infection.
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.
基金supported by the National Natural Sciences Foundation of China(81971473,82171753).
文摘Biological agents threats people's life through different ways,one of which lies in the impairment of cognition.It is believed cognitive decline may result from biological agents mediated neuron damage directly,or from the activation of the host immune response to eradicate the pathogen.However,direct linkage between infections and cognitive decline is very limited.Here we focus on the mechanisms of how different biological virus or they induced systemic and local inflammation link to the cognitive impairment,focusing on the roles of acti-vated microglia and several molecular pathways mediated neurotoxicity.
基金supported by the grants from the National Key Basic Research Program of China(2007CB512406)the National Natural Science Foundation of China(30571732)National"863"Fund Grant of China(2006AA02A254).
文摘The complement C5 anaphylatoxin receptor is a member of the seven transmembrane-spanning G protein-coupled receptor superfamily that signals through Gcxi and Gtz16. C5aR is mostly expressed on neutrophils, macrophages and endothelial cells. C5a and C5aR interaction plays an important role in numerous biological effects such as in vivo cytokine storm which results in inflammatory damage. Considering the limitation of collection of human peripheral blood neutrophils and their short half life, the stably transfected cell line for studying the biological effects of C5aR is needed. In this study, we transfected C5aR gene into Molt-4 cell line and examined the function of ectopic C5aR. Our results showed stable expression of the C5aR in Molt-4 cell line and their interaction with human C5a induced ERKI/2 phosphorylation, Ca＋＋ influx. This stable transfected cell line may provide a useful tool for studying signal pathways related to C5a and C5aR interplay and antibody development specific for C5aR. Cellular ＆ Molecular Immunology.
