{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wilkison M"],"funding":["NCRR NIH HHS","NHLBI NIH HHS"],"pagination":["151-62"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3388152"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["181(1)"],"pubmed_abstract":["HIV infection causes loss of CD4(+) T cells and type 1 interferon (IFN)-producing and IFN-responsive dendritic cells, resulting in immunodeficiencies and susceptibility to opportunistic infections, such as Pneumocystis. Osteoporosis and bone marrow failure are additional unexplained complications in HIV-positive patients and patients with AIDS, respectively. We recently demonstrated that mice that lack lymphocytes and IFN a/b receptor (IFrag(-/-)) develop bone marrow failure after Pneumocystis lung infection, whereas lymphocyte-deficient, IFN α/β receptor-competent mice (RAG(-/-)) had normal hematopoiesis. Interestingly, infected IFrag(-/-) mice also exhibited bone fragility, suggesting loss of bone mass. We quantified bone changes and evaluated the potential connection between progressing"],"journal":["The American journal of pathology"],"pubmed_title":["Type 1 interferons suppress accelerated osteoclastogenesis and prevent loss of bone mass during systemic inflammatory responses to Pneumocystis lung infection."],"pmcid":["PMC3388152"],"funding_grant_id":["P20 RR020185","R01HL090488","2P20RR020185-06","R01 HL090488"],"pubmed_authors":["Wilkison M","Gauss K","Meissner N","Searles S","Taylor D","Ran Y"],"additional_accession":[]},"is_claimable":false,"name":"Type 1 interferons suppress accelerated osteoclastogenesis and prevent loss of bone mass during systemic inflammatory responses to Pneumocystis lung infection.","description":"HIV infection causes loss of CD4(+) T cells and type 1 interferon (IFN)-producing and IFN-responsive dendritic cells, resulting in immunodeficiencies and susceptibility to opportunistic infections, such as Pneumocystis. Osteoporosis and bone marrow failure are additional unexplained complications in HIV-positive patients and patients with AIDS, respectively. We recently demonstrated that mice that lack lymphocytes and IFN a/b receptor (IFrag(-/-)) develop bone marrow failure after Pneumocystis lung infection, whereas lymphocyte-deficient, IFN α/β receptor-competent mice (RAG(-/-)) had normal hematopoiesis. Interestingly, infected IFrag(-/-) mice also exhibited bone fragility, suggesting loss of bone mass. We quantified bone changes and evaluated the potential connection between progressing","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 Jul","modification":"2025-04-05T13:20:02.298Z","creation":"2019-03-27T00:55:09Z"},"accession":"S-EPMC3388152","cross_references":{"pubmed":["22626807"],"doi":["10.1016/j.ajpath.2012.03.023"]}}