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© Research
Publication : Kidney international

Glomerular common gamma chain confers B- and T-cell-independent protection against glomerulonephritis

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Kidney international - 19 Jan 2017

Luque Y, Cathelin D, Vandermeersch S, Xu X, Sohier J, Placier S, Xu-Dubois YC, Louis K, Hertig A, Bories JC, Vasseur F, Campagne F, Di Santo JP, Vosshenrich C, Rondeau E, Mesnard L

Link to Pubmed [PMID] – 28111009

Kidney Int. 2017 May;91(5):1146-1158

Crescentic glomerulonephritis is a life-threatening renal disease that has been extensively studied by the experimental anti-glomerular basement membrane glomerulonephritis (anti-GBM-GN) model. Although T cells have a significant role in this model, athymic/nude mice and rats still develop severe renal disease. Here we further explored the contribution of intrinsic renal cells in the development of T-cell-independent GN lesions. Anti-GBM-GN was induced in three strains of immune-deficient mice (Rag2, Rag2Il2rg, and Rag2Il2rb) that are devoid of either T/B cells or T/B/NK cells. The Rag2Il2rg or Rag2Il2rb mice harbor an additional deletion of either the common gamma chain (γC) or the interleukin-2 receptor β subunit (IL-2Rβ), respectively, impairing IL-15 signaling in particular. As expected, all these strains developed severe anti-GBM-GN. Additionally, bone marrow replenishment experiments allowed us to deduce a protective role for the glomerular-expressed γC during anti-GBM-GN. Given that IL-15 has been found highly expressed in nephritic kidneys despite the absence of lymphocytes, we then studied this cytokine in vitro on primary cultured podocytes from immune-deficient mice (Rag2Il2rg and Rag2Il2rb) compared to controls. IL-15 induced downstream activation of JAK1/3 and SYK in primary cultured podocytes. IL-15-dependent JAK/SYK induction was impaired in the absence of γC or IL-2Rβ. We found γC largely induced on podocytes during human glomerulonephritis. Thus, renal lesions are indeed modulated by intrinsic glomerular cells through the γC/IL-2Rβ receptor response, to date classically described only in immune cells.

https://www.ncbi.nlm.nih.gov/pubmed/28111009