{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Atif SM"],"funding":["NIH"],"pagination":["125494"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6629102"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["5"],"pubmed_abstract":["Susceptibility to chronic beryllium (Be) disease is linked to HLA-DP molecules possessing a glutamic acid at the 69th position of the β-chain (βGlu69), with the most prevalent βGlu69-containing molecule being HLA-DP2. We have previously shown that HLA-DP2 transgenic (Tg) mice exposed to Be oxide (BeO) develop mononuclear infiltrates in a peribronchovascular distribution and a beryllium-specific, HLA-DP2-restricted CD4+ T cell response. In addition to T cells, B cells constituted a major portion of infiltrated leukocytes in the lung of BeO-exposed HLA-DP2 Tg mice and sequester BeO particles within ectopic lymphoid aggregates and granulomas. B cell depletion was associated with a loss of lymphoid aggregates and granulomas as well as a significant increase in lung injury in BeO-exposed mice. The protective role of B cells was innate in origin, and BeO-induced B cell recruitment to the lung was dependent on MyD88 signaling. Similar to BeO-exposed HLA-DP2 mice, B cells also accumulate in the lungs of CBD subjects, located at the periphery and surrounding the granuloma. Overall, our data suggest a novel modulatory role for B cells in the protection of the lung against sterile particulate exposure, with B cell recruitment to the inflamed lung occurring in an antigen-independent and MyD88-dependent manner."],"journal":["JCI insight"],"pubmed_title":["Protective role of B cells in sterile particulate-induced lung injury."],"pmcid":["PMC6629102"],"funding_grant_id":["ES025534,HL062410,HL102245"],"pubmed_authors":["McKee AS","Rangel-Moreno J","Tuder R","Maier LA","Martin AK","Atif SM","Mack DG","Getahun A","Fontenot AP","Cambier JC"],"additional_accession":[]},"is_claimable":false,"name":"Protective role of B cells in sterile particulate-induced lung injury.","description":"Susceptibility to chronic beryllium (Be) disease is linked to HLA-DP molecules possessing a glutamic acid at the 69th position of the β-chain (βGlu69), with the most prevalent βGlu69-containing molecule being HLA-DP2. We have previously shown that HLA-DP2 transgenic (Tg) mice exposed to Be oxide (BeO) develop mononuclear infiltrates in a peribronchovascular distribution and a beryllium-specific, HLA-DP2-restricted CD4+ T cell response. In addition to T cells, B cells constituted a major portion of infiltrated leukocytes in the lung of BeO-exposed HLA-DP2 Tg mice and sequester BeO particles within ectopic lymphoid aggregates and granulomas. B cell depletion was associated with a loss of lymphoid aggregates and granulomas as well as a significant increase in lung injury in BeO-exposed mice. The protective role of B cells was innate in origin, and BeO-induced B cell recruitment to the lung was dependent on MyD88 signaling. Similar to BeO-exposed HLA-DP2 mice, B cells also accumulate in the lungs of CBD subjects, located at the periphery and surrounding the granuloma. Overall, our data suggest a novel modulatory role for B cells in the protection of the lung against sterile particulate exposure, with B cell recruitment to the inflamed lung occurring in an antigen-independent and MyD88-dependent manner.","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 May","modification":"2025-04-04T21:27:17.315Z","creation":"2019-07-25T07:09:58Z"},"accession":"S-EPMC6629102","cross_references":{"pubmed":["31094704"],"doi":["10.1172/jci.insight.125494"]}}