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10.4049/jimmunol.169.11.6193 http://scihub22266oqcxt.onion/10.4049/jimmunol.169.11.6193 12444124!ä!12444124 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=12444124&cmd=llinks): Failed to open stream: HTTP request failed! 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Bone marrow B cell apoptosis during in vivo influenza virus infection requires TNF-alpha and lymphotoxin-alpha |pdf=|usr=}}{{12444124}} gab.com Text Bone marrow B cell apoptosis during in vivo influenza virus infection requires TNF-alpha and lymphotoxin-alpha JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=12444124 #FOAvip Suppression of bone marrow myeloid and erythroid progenitor cells occurs after infection with a variety of different viruses. In this study, we characterize the alterations in bone marrow (BM) lymphocytes after influenza virus infection in mice. We found a severe loss of BM B cells, particularly CD43(low/-)B220(+) pre-B and immature B cells, in influenza virus-infected mice. Depletion of BM B lineage cells resulted primarily from cell cycle arrest and most likely apoptosis within the BM environment, rather than from increased trafficking of BM emigrants to peripheral lymphoid tissues. Use of gene-knockout mice indicates that depletion of BM B cells is dependent on TNF-alpha, lymphotoxin-alpha, and both TNF receptors, TNFR1-p55 and TNFR2-p75. Thus, TNF-alpha and lymphotoxin-alpha are required for loss of BM B lineage cells during respiratory infection with influenza virus. Twit Text FOAVip Bone marrow B cell apoptosis during in vivo influenza virus infection requires TNF-alpha and lymphotoxin-alpha ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=12444124 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=12444124 #FOAvip English Wikipedia <ref>{{Cite pmid|12444124}}</ref> Bone marrow B cell apoptosis during in vivo influenza virus infection requires TNF-alpha and lymphotoxin-alpha #MMPMID12444124 Sedger LM; Hou S; Osvath SR; Glaccum MB; Peschon JJ; van Rooijen N; Hyland L J Immunol 2002[Dec]; 169 (11): 6193-201 PMID12444124show ga Suppression of bone marrow myeloid and erythroid progenitor cells occurs after infection with a variety of different viruses. In this study, we characterize the alterations in bone marrow (BM) lymphocytes after influenza virus infection in mice. We found a severe loss of BM B cells, particularly CD43(low/-)B220(+) pre-B and immature B cells, in influenza virus-infected mice. Depletion of BM B lineage cells resulted primarily from cell cycle arrest and most likely apoptosis within the BM environment, rather than from increased trafficking of BM emigrants to peripheral lymphoid tissues. Use of gene-knockout mice indicates that depletion of BM B cells is dependent on TNF-alpha, lymphotoxin-alpha, and both TNF receptors, TNFR1-p55 and TNFR2-p75. Thus, TNF-alpha and lymphotoxin-alpha are required for loss of BM B lineage cells during respiratory infection with influenza virus. |Animals[MESH] |Antigens, CD/genetics/metabolism[MESH] |Apoptosis/*immunology[MESH] |B-Lymphocytes/*immunology/*pathology[MESH] |Base Sequence[MESH] |Bone Marrow Cells/immunology/pathology[MESH] |Cell Cycle[MESH] |Cell Differentiation[MESH] |Killer Cells, Natural/immunology[MESH] |Kinetics[MESH] |Lymphotoxin-alpha/deficiency/genetics/*metabolism[MESH] |Macrophages, Alveolar/immunology[MESH] |Mice[MESH] |Mice, Inbred BALB C[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Orthomyxoviridae Infections/*immunology/*pathology/virology[MESH] |Orthomyxoviridae/pathogenicity/physiology[MESH] |RNA, Messenger/genetics/metabolism[MESH] |Receptors, Tumor Necrosis Factor, Type I[MESH] |Receptors, Tumor Necrosis Factor, Type II[MESH] |Receptors, Tumor Necrosis Factor/deficiency/genetics/metabolism[MESH] |T-Lymphocyte Subsets/immunology[MESH] |Tumor Necrosis Factor-alpha/deficiency/genetics/*metabolism[MESH]Bone marrow B cell apoptosis during in vivo influenza virus infection (epmc).pdf DeepDyve Pubget Overpricing