| First Author | Zein HS | Year | 2022 |
| Journal | Sci Rep | Volume | 12 |
| Issue | 1 | Pages | 4834 |
| PubMed ID | 35318366 | Mgi Jnum | J:322835 |
| Mgi Id | MGI:7259616 | Doi | 10.1038/s41598-022-08547-9 |
| Citation | Zein HS, et al. (2022) Clr-f expression regulates kidney immune and metabolic homeostasis. Sci Rep 12(1):4834 |
| abstractText | 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(-/-)) 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(-/-) 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(-/-) mouse kidneys identified elevated IL-12 and IFNgamma in cells of the tubulointerstitium, and an infiltrating population of neutrophils and T and B lymphocytes. The presence of these insults in a Rag1(-/-)Clr-f(-/-) background reveals that Clr-f(-/-) 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. |
