{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zein HS"],"funding":["Kidney Foundation of Canada"],"pagination":["4834"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8940912"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(1)"],"pubmed_abstract":["The C-type lectin-related protein, Clr-f, encoded by Clec2h in the mouse NK gene complex (NKC), is a member of a family of immune regulatory lectins that guide immune responses at distinct tissues of the body. Clr-f is highly expressed in the kidney; however, its activity in this organ is unknown. To assess the requirement for Clr-f in kidney health and function, we generated a Clr-f-deficient mouse (Clr-f<sup>-/-</sup>) by targeted deletions in the Clec2h gene. Mice lacking Clr-f exhibited glomerular and tubular lesions, immunoglobulin and C3 complement protein renal deposits, and significant abdominal and ectopic lipid accumulation. Whole kidney transcriptional profile analysis of Clr-f<sup>-/-</sup> mice at 7, 13, and 24 weeks of age revealed a dynamic dysregulation in lipid metabolic processes, stress responses, and inflammatory mediators. Examination of the immune contribution to the pathologies of Clr-f<sup>-/-</sup> mouse kidneys identified elevated IL-12 and IFNγ in cells of the tubulointerstitium, and an infiltrating population of neutrophils and T and B lymphocytes. The presence of these insults in a Rag1<sup>-/-</sup>Clr-f<sup>-/-</sup> background reveals that Clr-f<sup>-/-</sup> mice are susceptible to a T and B lymphocyte-independent renal pathogenesis. Our data reveal a role for Clr-f in the maintenance of kidney immune and metabolic homeostasis."],"journal":["Scientific reports"],"pubmed_title":["Clr-f expression regulates kidney immune and metabolic homeostasis."],"pmcid":["PMC8940912"],"funding_grant_id":["KFOC 190027"],"pubmed_authors":["Parsons BD","Medina-Luna D","Pelino TJ","Gutsol A","Makrigiannis AP","Hall CW","Gamage GS","Abou-Samra E","Scur M","Abujamel T","Steinle A","Dasgupta B","Rahim MMA","Zein HS","Gharibeh L","Nemer M"],"additional_accession":[]},"is_claimable":false,"name":"Clr-f expression regulates kidney immune and metabolic homeostasis.","description":"The C-type lectin-related protein, Clr-f, encoded by Clec2h in the mouse NK gene complex (NKC), is a member of a family of immune regulatory lectins that guide immune responses at distinct tissues of the body. Clr-f is highly expressed in the kidney; however, its activity in this organ is unknown. To assess the requirement for Clr-f in kidney health and function, we generated a Clr-f-deficient mouse (Clr-f<sup>-/-</sup>) by targeted deletions in the Clec2h gene. Mice lacking Clr-f exhibited glomerular and tubular lesions, immunoglobulin and C3 complement protein renal deposits, and significant abdominal and ectopic lipid accumulation. Whole kidney transcriptional profile analysis of Clr-f<sup>-/-</sup> mice at 7, 13, and 24 weeks of age revealed a dynamic dysregulation in lipid metabolic processes, stress responses, and inflammatory mediators. Examination of the immune contribution to the pathologies of Clr-f<sup>-/-</sup> mouse kidneys identified elevated IL-12 and IFNγ in cells of the tubulointerstitium, and an infiltrating population of neutrophils and T and B lymphocytes. The presence of these insults in a Rag1<sup>-/-</sup>Clr-f<sup>-/-</sup> background reveals that Clr-f<sup>-/-</sup> mice are susceptible to a T and B lymphocyte-independent renal pathogenesis. Our data reveal a role for Clr-f in the maintenance of kidney immune and metabolic homeostasis.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Mar","modification":"2025-04-22T18:19:47.908Z","creation":"2025-04-06T02:23:19.633Z"},"accession":"S-EPMC8940912","cross_references":{"pubmed":["35318366"],"doi":["10.1038/s41598-022-08547-9"]}}