<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wilkison M</submitter><funding>NCRR NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>151-62</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3388152</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>181(1)</volume><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</pubmed_abstract><journal>The American journal of pathology</journal><pubmed_title>Type 1 interferons suppress accelerated osteoclastogenesis and prevent loss of bone mass during systemic inflammatory responses to Pneumocystis lung infection.</pubmed_title><pmcid>PMC3388152</pmcid><funding_grant_id>P20 RR020185</funding_grant_id><funding_grant_id>R01HL090488</funding_grant_id><funding_grant_id>2P20RR020185-06</funding_grant_id><funding_grant_id>R01 HL090488</funding_grant_id><pubmed_authors>Wilkison M</pubmed_authors><pubmed_authors>Gauss K</pubmed_authors><pubmed_authors>Meissner N</pubmed_authors><pubmed_authors>Searles S</pubmed_authors><pubmed_authors>Taylor D</pubmed_authors><pubmed_authors>Ran Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Type 1 interferons suppress accelerated osteoclastogenesis and prevent loss of bone mass during systemic inflammatory responses to Pneumocystis lung infection.</name><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</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 Jul</publication><modification>2025-04-05T13:20:02.298Z</modification><creation>2019-03-27T00:55:09Z</creation></dates><accession>S-EPMC3388152</accession><cross_references><pubmed>22626807</pubmed><doi>10.1016/j.ajpath.2012.03.023</doi></cross_references></HashMap>