Dimethyl itaconate inhibits LPS-induced inflammatory release and apoptosis in alveolar type II epithelial and bronchial epithelial cells by activating pulmonary surfactant proteins A and D
CONCLUSION: The findings of the present study revealed that DMI inhibited LPS-induced inflammatory release and apoptosis in cells by targeting SIRT1 and then activating SP-A and SP-D. This novel insight into the pharmacological mechanism of DMI lays the foundation for its later use for alleviating lung injury.PMID:36335462 | DOI:10.15586/aei.v50i6.586 (Source: Allergologia et Immunopathologia)
Source: Allergologia et Immunopathologia - November 6, 2022 Category: Allergy & Immunology Authors: Yun Shi Huai-Qing Yin Source Type: research
Dimethyl itaconate inhibits LPS-induced inflammatory release and apoptosis in alveolar type II epithelial and bronchial epithelial cells by activating pulmonary surfactant proteins A and D
CONCLUSION: The findings of the present study revealed that DMI inhibited LPS-induced inflammatory release and apoptosis in cells by targeting SIRT1 and then activating SP-A and SP-D. This novel insight into the pharmacological mechanism of DMI lays the foundation for its later use for alleviating lung injury.PMID:36335462 | DOI:10.15586/aei.v50i6.586 (Source: Allergologia et Immunopathologia)
Source: Allergologia et Immunopathologia - November 6, 2022 Category: Allergy & Immunology Authors: Yun Shi Huai-Qing Yin Source Type: research
Dimethyl itaconate inhibits LPS-induced inflammatory release and apoptosis in alveolar type II epithelial and bronchial epithelial cells by activating pulmonary surfactant proteins A and D
CONCLUSION: The findings of the present study revealed that DMI inhibited LPS-induced inflammatory release and apoptosis in cells by targeting SIRT1 and then activating SP-A and SP-D. This novel insight into the pharmacological mechanism of DMI lays the foundation for its later use for alleviating lung injury.PMID:36335462 | DOI:10.15586/aei.v50i6.586 (Source: Allergologia et Immunopathologia)
Source: Allergologia et Immunopathologia - November 6, 2022 Category: Allergy & Immunology Authors: Yun Shi Huai-Qing Yin Source Type: research
Dimethyl itaconate inhibits LPS-induced inflammatory release and apoptosis in alveolar type II epithelial and bronchial epithelial cells by activating pulmonary surfactant proteins A and D
CONCLUSION: The findings of the present study revealed that DMI inhibited LPS-induced inflammatory release and apoptosis in cells by targeting SIRT1 and then activating SP-A and SP-D. This novel insight into the pharmacological mechanism of DMI lays the foundation for its later use for alleviating lung injury.PMID:36335462 | DOI:10.15586/aei.v50i6.586 (Source: Allergologia et Immunopathologia)
Source: Allergologia et Immunopathologia - November 6, 2022 Category: Allergy & Immunology Authors: Yun Shi Huai-Qing Yin Source Type: research
Dimethyl itaconate inhibits LPS-induced inflammatory release and apoptosis in alveolar type II epithelial and bronchial epithelial cells by activating pulmonary surfactant proteins A and D
CONCLUSION: The findings of the present study revealed that DMI inhibited LPS-induced inflammatory release and apoptosis in cells by targeting SIRT1 and then activating SP-A and SP-D. This novel insight into the pharmacological mechanism of DMI lays the foundation for its later use for alleviating lung injury.PMID:36335462 | DOI:10.15586/aei.v50i6.586 (Source: Allergologia et Immunopathologia)
Source: Allergologia et Immunopathologia - November 6, 2022 Category: Allergy & Immunology Authors: Yun Shi Huai-Qing Yin Source Type: research
Dimethyl itaconate inhibits LPS-induced inflammatory release and apoptosis in alveolar type II epithelial and bronchial epithelial cells by activating pulmonary surfactant proteins A and D
CONCLUSION: The findings of the present study revealed that DMI inhibited LPS-induced inflammatory release and apoptosis in cells by targeting SIRT1 and then activating SP-A and SP-D. This novel insight into the pharmacological mechanism of DMI lays the foundation for its later use for alleviating lung injury.PMID:36335462 | DOI:10.15586/aei.v50i6.586 (Source: Allergologia et Immunopathologia)
Source: Allergologia et Immunopathologia - November 6, 2022 Category: Allergy & Immunology Authors: Yun Shi Huai-Qing Yin Source Type: research
Dimethyl itaconate inhibits LPS-induced inflammatory release and apoptosis in alveolar type II epithelial and bronchial epithelial cells by activating pulmonary surfactant proteins A and D
CONCLUSION: The findings of the present study revealed that DMI inhibited LPS-induced inflammatory release and apoptosis in cells by targeting SIRT1 and then activating SP-A and SP-D. This novel insight into the pharmacological mechanism of DMI lays the foundation for its later use for alleviating lung injury.PMID:36335462 | DOI:10.15586/aei.v50i6.586 (Source: Allergologia et Immunopathologia)
Source: Allergologia et Immunopathologia - November 6, 2022 Category: Allergy & Immunology Authors: Yun Shi Huai-Qing Yin Source Type: research
Dimethyl itaconate inhibits LPS-induced inflammatory release and apoptosis in alveolar type II epithelial and bronchial epithelial cells by activating pulmonary surfactant proteins A and D
CONCLUSION: The findings of the present study revealed that DMI inhibited LPS-induced inflammatory release and apoptosis in cells by targeting SIRT1 and then activating SP-A and SP-D. This novel insight into the pharmacological mechanism of DMI lays the foundation for its later use for alleviating lung injury.PMID:36335462 | DOI:10.15586/aei.v50i6.586 (Source: Allergologia et Immunopathologia)
Source: Allergologia et Immunopathologia - November 6, 2022 Category: Allergy & Immunology Authors: Yun Shi Huai-Qing Yin Source Type: research
Dimethyl itaconate inhibits LPS-induced inflammatory release and apoptosis in alveolar type II epithelial and bronchial epithelial cells by activating pulmonary surfactant proteins A and D
CONCLUSION: The findings of the present study revealed that DMI inhibited LPS-induced inflammatory release and apoptosis in cells by targeting SIRT1 and then activating SP-A and SP-D. This novel insight into the pharmacological mechanism of DMI lays the foundation for its later use for alleviating lung injury.PMID:36335462 | DOI:10.15586/aei.v50i6.586 (Source: Allergologia et Immunopathologia)
Source: Allergologia et Immunopathologia - November 6, 2022 Category: Allergy & Immunology Authors: Yun Shi Huai-Qing Yin Source Type: research
Dimethyl itaconate inhibits LPS-induced inflammatory release and apoptosis in alveolar type II epithelial and bronchial epithelial cells by activating pulmonary surfactant proteins A and D
CONCLUSION: The findings of the present study revealed that DMI inhibited LPS-induced inflammatory release and apoptosis in cells by targeting SIRT1 and then activating SP-A and SP-D. This novel insight into the pharmacological mechanism of DMI lays the foundation for its later use for alleviating lung injury.PMID:36335462 | DOI:10.15586/aei.v50i6.586 (Source: Allergologia et Immunopathologia)
Source: Allergologia et Immunopathologia - November 6, 2022 Category: Allergy & Immunology Authors: Yun Shi Huai-Qing Yin Source Type: research
Dimethyl itaconate inhibits LPS-induced inflammatory release and apoptosis in alveolar type II epithelial and bronchial epithelial cells by activating pulmonary surfactant proteins A and D
CONCLUSION: The findings of the present study revealed that DMI inhibited LPS-induced inflammatory release and apoptosis in cells by targeting SIRT1 and then activating SP-A and SP-D. This novel insight into the pharmacological mechanism of DMI lays the foundation for its later use for alleviating lung injury.PMID:36335462 | DOI:10.15586/aei.v50i6.586 (Source: Allergologia et Immunopathologia)
Source: Allergologia et Immunopathologia - November 6, 2022 Category: Allergy & Immunology Authors: Yun Shi Huai-Qing Yin Source Type: research
Dimethyl itaconate inhibits LPS-induced inflammatory release and apoptosis in alveolar type II epithelial and bronchial epithelial cells by activating pulmonary surfactant proteins A and D
CONCLUSION: The findings of the present study revealed that DMI inhibited LPS-induced inflammatory release and apoptosis in cells by targeting SIRT1 and then activating SP-A and SP-D. This novel insight into the pharmacological mechanism of DMI lays the foundation for its later use for alleviating lung injury.PMID:36335462 | DOI:10.15586/aei.v50i6.586 (Source: Allergologia et Immunopathologia)
Source: Allergologia et Immunopathologia - November 6, 2022 Category: Allergy & Immunology Authors: Yun Shi Huai-Qing Yin Source Type: research
The present and future of immunocytokines for cancer treatment
Cell Mol Life Sci. 2022 Sep 6;79(10):509. doi: 10.1007/s00018-022-04514-9.ABSTRACTMonoclonal antibody (mAb) therapy has successfully been introduced as treatment of several lymphomas and leukemias. However, solid tumors reduce the efficacy of mAb therapy because of an immune-suppressive tumor micro-environment (TME), which hampers activation of effector immune cells. Pro-inflammatory cytokine therapy may counteract immune suppression in the TME and increase mAb efficacy, but untargeted pro-inflammatory cytokine therapy is limited by severe off-target toxicity and a short half-life of cytokines. Antibody-cytokine fusion pro...
Source: Cellular and Molecular Life Sciences : CMLS - September 6, 2022 Category: Cytology Authors: Dennis Y Gout Lotte S Groen Marjolein van Egmond Source Type: research
The present and future of immunocytokines for cancer treatment
Cell Mol Life Sci. 2022 Sep 6;79(10):509. doi: 10.1007/s00018-022-04514-9.ABSTRACTMonoclonal antibody (mAb) therapy has successfully been introduced as treatment of several lymphomas and leukemias. However, solid tumors reduce the efficacy of mAb therapy because of an immune-suppressive tumor micro-environment (TME), which hampers activation of effector immune cells. Pro-inflammatory cytokine therapy may counteract immune suppression in the TME and increase mAb efficacy, but untargeted pro-inflammatory cytokine therapy is limited by severe off-target toxicity and a short half-life of cytokines. Antibody-cytokine fusion pro...
Source: Cellular and Molecular Life Sciences : CMLS - September 6, 2022 Category: Cytology Authors: Dennis Y Gout Lotte S Groen Marjolein van Egmond Source Type: research
The present and future of immunocytokines for cancer treatment
Cell Mol Life Sci. 2022 Sep 6;79(10):509. doi: 10.1007/s00018-022-04514-9.ABSTRACTMonoclonal antibody (mAb) therapy has successfully been introduced as treatment of several lymphomas and leukemias. However, solid tumors reduce the efficacy of mAb therapy because of an immune-suppressive tumor micro-environment (TME), which hampers activation of effector immune cells. Pro-inflammatory cytokine therapy may counteract immune suppression in the TME and increase mAb efficacy, but untargeted pro-inflammatory cytokine therapy is limited by severe off-target toxicity and a short half-life of cytokines. Antibody-cytokine fusion pro...
Source: Cellular and Molecular Life Sciences : CMLS - September 6, 2022 Category: Cytology Authors: Dennis Y Gout Lotte S Groen Marjolein van Egmond Source Type: research
