The Experts below are selected from a list of 6906 Experts worldwide ranked by ideXlab platform
Irene Garcia - One of the best experts on this subject based on the ideXlab platform.
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transmembrane tnf and partially tnfr1 regulate tnfr2 expression and control inflammation in mycobacterial induced pleurisy
International Journal of Molecular Sciences, 2018Co-Authors: Husnu Uysal, Leslie Chavezgalan, Dominique Vesin, Guillaume Blaser, Mahdia Benkhoucha, Bernhard Ryffel, Valerie F J Quesniaux, Irene GarciaAbstract:Pleural tuberculosis is one of the most frequent forms of extra-pulmonary tuberculosis observed in patients infected with Mycobacterium tuberculosis. Tumor Necrosis Factor (TNF) is a crucial cytokine needed to control tuberculosis infection that remains a leading cause of morbidity and mortality worldwide. TNF blockade compromises host immunity and may increase the risk of reactivation of latent infection resulting in overt pulmonary, Pleural and extra-pulmonary tuberculosis. While TNF signaling is mainly considered pro-inflammatory, its requirement for the anti-inflammation process involved in the resolution of infection and tissue repair is less explored. Our study analyzes the role of TNF and TNF receptors in the control of the inflammatory process associated with Bacillus Calmette-Guerin (BCG)-induced pleurisy. This study shows that the absence of TNF causes exacerbated inflammation in the Pleural Cavity of BCG-infected mice which is controlled by the transmembrane TNF (tmTNF) expression. The lack of TNF is associated with an impaired cellular expression and shedding of TNFR2 in the Pleural Cavity. The presence of tmTNF restores the normal expression of TNFR2 on myeloid cells during BCG-induced pleurisy. We also show that absence of TNFR1 affects the expression of TNFR2 on Pleural cells and inflammation in the Pleural Cavity of BCG-infected mice. In conclusion, tmTNF but not soluble TNF prevents Pleural Cavity inflammation leading to attenuation and the resolution of the inflammatory process caused by mycobacterial pleurisy in association with the expression of TNFR2 on myeloid cells.
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transmembrane tumor necrosis factor controls myeloid derived suppressor cell activity via tnf receptor 2 and protects from excessive inflammation during bcg induced pleurisy
Frontiers in Immunology, 2017Co-Authors: Leslie Chavezgalan, Husnu Uysal, Dominique Vesin, Guillaume Blaser, Mahdia Benkhoucha, Bernhard Ryffel, Valerie F J Quesniaux, Irene GarciaAbstract:Pleural tuberculosis (TB) is a form of extra-pulmonary TB observed in patients infected with Mycobacterium tuberculosis. Accumulation of myeloid-derived suppressor cells (MDSC) has been observed in animal models of TB and in human patients but their role remains to be fully elucidated. In this study, we analyzed the role of transmembrane TNF (tmTNF) in the accumulation and function of MDSC in the Pleural Cavity during an acute mycobacterial infection. M. bovis BCG-induced pleurisy was resolved in mice expressing tmTNF, but lethal in the absence of TNF. Pleural infection induced MDSC accumulation in the Pleural Cavity and functional MDSC required tmTNF to suppress T cells as did Pleural WT MDSC. Interaction of MDSC expressing tmTNF with CD4 T cells bearing TNFR2, but not TNFR1, was required for MDSC suppressive activity on CD4 T cells. Expression of tmTNF attenuated Th1 cell-mediated inflammatory responses generated by the acute Pleural mycobacterial infection in association with effective MDSC expressing tmTNF and interacting with CD4 T cells expressing TNFR2. In conclusion, this study provides new insights into the crucial role played by the tmTNF/TNFR2 pathway in MDSC suppressive activity required during acute Pleural infection to attenuate excessive inflammation generated by the infection.
Hiroshi Honda - One of the best experts on this subject based on the ideXlab platform.
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mri of retroperitoneal solitary fibrous tumor in the suprarenal region
American Journal of Roentgenology, 2007Co-Authors: Daisuke Kakihara, Kengo Yoshimitsu, Shuji Matsuura, Hiroshi HondaAbstract:WEB This is a Web exclusive article. olitary fibrous tumor (SFT) is a rare tumor usually originating in the Pleural Cavity. ExtraPleural SFTs have been found in various regions of the body. The retroperitoneum is one of the relatively frequent regions in which SFTs are found, 28 cases having been reported so far, but the radiologic features have rarely been described. To our knowledge this report is the first of MRI findings on SFT originating in the periadrenal region.
Periklis Tomos - One of the best experts on this subject based on the ideXlab platform.
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a rupture of a huge thymic cyst into the Pleural Cavity a case report
Respiratory Medicine, 2006Co-Authors: E Lachanas, P Konofaos, G Irba, Periklis TomosAbstract:Summary Thymic cysts (TCs) represent 1–2% of all mediastinal masses. To the best of our knowledge transudative effusion due to rupture of a TC into the Pleural Cavity, as it happened with our patient, has never been described before. The patient was admitted in 5th Department of Respiratory Medicine of "SOTIRIA" Hospital complaining of pleuritic chest pain in the right hemithorax and dyspnea on exertion. Clinical and laboratory examinations indicated a right Pleural effusion. Then, the patient was transferred to the 2nd Department of Propedeutic Surgery of ‘LAIKO’ Hospital where he underwent surgery. Video-assisted thoracic surgery (VATS) revealed an enormous 25-cm cyst ruptured into the right Pleural Cavity. The cyst was removed by open thoracotomy due to adhesion to contiguous tissues. Pathological examination indicated thymic origins
Andre Rizk - One of the best experts on this subject based on the ideXlab platform.
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thoracoscopic management of a pericardial migration of a breast biopsy localization wire
The Annals of Thoracic Surgery, 2009Co-Authors: Fouad M Azoury, Paul Sayad, Andre RizkAbstract:Intrathoracic migration of a breast biopsy localization wire is relatively rare and most of the wires end up in the Pleural Cavity. We report the first case of almost total intrapericardial migration of a monofilament hooked wire that was lost during the breast biopsy procedure. The case was successfully managed by video-assisted thoracoscopic surgery. Postulated mechanisms of migration of such wires are reviewed and a new mechanism is proposed.
Valerie F J Quesniaux - One of the best experts on this subject based on the ideXlab platform.
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transmembrane tnf and partially tnfr1 regulate tnfr2 expression and control inflammation in mycobacterial induced pleurisy
International Journal of Molecular Sciences, 2018Co-Authors: Husnu Uysal, Leslie Chavezgalan, Dominique Vesin, Guillaume Blaser, Mahdia Benkhoucha, Bernhard Ryffel, Valerie F J Quesniaux, Irene GarciaAbstract:Pleural tuberculosis is one of the most frequent forms of extra-pulmonary tuberculosis observed in patients infected with Mycobacterium tuberculosis. Tumor Necrosis Factor (TNF) is a crucial cytokine needed to control tuberculosis infection that remains a leading cause of morbidity and mortality worldwide. TNF blockade compromises host immunity and may increase the risk of reactivation of latent infection resulting in overt pulmonary, Pleural and extra-pulmonary tuberculosis. While TNF signaling is mainly considered pro-inflammatory, its requirement for the anti-inflammation process involved in the resolution of infection and tissue repair is less explored. Our study analyzes the role of TNF and TNF receptors in the control of the inflammatory process associated with Bacillus Calmette-Guerin (BCG)-induced pleurisy. This study shows that the absence of TNF causes exacerbated inflammation in the Pleural Cavity of BCG-infected mice which is controlled by the transmembrane TNF (tmTNF) expression. The lack of TNF is associated with an impaired cellular expression and shedding of TNFR2 in the Pleural Cavity. The presence of tmTNF restores the normal expression of TNFR2 on myeloid cells during BCG-induced pleurisy. We also show that absence of TNFR1 affects the expression of TNFR2 on Pleural cells and inflammation in the Pleural Cavity of BCG-infected mice. In conclusion, tmTNF but not soluble TNF prevents Pleural Cavity inflammation leading to attenuation and the resolution of the inflammatory process caused by mycobacterial pleurisy in association with the expression of TNFR2 on myeloid cells.
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transmembrane tumor necrosis factor controls myeloid derived suppressor cell activity via tnf receptor 2 and protects from excessive inflammation during bcg induced pleurisy
Frontiers in Immunology, 2017Co-Authors: Leslie Chavezgalan, Husnu Uysal, Dominique Vesin, Guillaume Blaser, Mahdia Benkhoucha, Bernhard Ryffel, Valerie F J Quesniaux, Irene GarciaAbstract:Pleural tuberculosis (TB) is a form of extra-pulmonary TB observed in patients infected with Mycobacterium tuberculosis. Accumulation of myeloid-derived suppressor cells (MDSC) has been observed in animal models of TB and in human patients but their role remains to be fully elucidated. In this study, we analyzed the role of transmembrane TNF (tmTNF) in the accumulation and function of MDSC in the Pleural Cavity during an acute mycobacterial infection. M. bovis BCG-induced pleurisy was resolved in mice expressing tmTNF, but lethal in the absence of TNF. Pleural infection induced MDSC accumulation in the Pleural Cavity and functional MDSC required tmTNF to suppress T cells as did Pleural WT MDSC. Interaction of MDSC expressing tmTNF with CD4 T cells bearing TNFR2, but not TNFR1, was required for MDSC suppressive activity on CD4 T cells. Expression of tmTNF attenuated Th1 cell-mediated inflammatory responses generated by the acute Pleural mycobacterial infection in association with effective MDSC expressing tmTNF and interacting with CD4 T cells expressing TNFR2. In conclusion, this study provides new insights into the crucial role played by the tmTNF/TNFR2 pathway in MDSC suppressive activity required during acute Pleural infection to attenuate excessive inflammation generated by the infection.