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B cell subsets contribute to renal injury and renal protection after ischemia/reperfusion (CROSBI ID 180137)

Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija

Renner, B. ; ... ; Ljubanović, D. ; ... ; Thurman, J.M. B cell subsets contribute to renal injury and renal protection after ischemia/reperfusion // Journal of immunology, 185 (2010), 7; 4393-4400. doi: 10.4049/jimmunol.0903239

Podaci o odgovornosti

Renner, B. ; ... ; Ljubanović, D. ; ... ; Thurman, J.M.

engleski

B cell subsets contribute to renal injury and renal protection after ischemia/reperfusion

Ischemia/reperfusion (I/R) triggers a robust inflammatory response within the kidney. Numerous components of the immune system contribute to the resultant renal injury, including the complement system. We sought to identify whether natural Abs bind to the postischemic kidney and contribute to complement activation after I/R.We depleted peritoneal B cells in mice by hypotonic shock. Depletion of the peritoneal B cells prevented the deposition of IgM within the glomeruli after renal I/R and attenuated renal injury after I/R.We found that glomerular IgM activates the classical pathway of complement, but it does not cause substantial deposition of C3 within the kidney. Furthermore, mice deficient in classical pathway proteins were not protected from injury, indicating that glomerular IgM does not cause injury through activation of the classical pathway. We also subjected mice deficient in all mature B cells (mMT mice) to renal I/R and found that they sustained worse renal injury than wild-type controls. Serum IL-10 levels were lower in the mMT mice. Taken together, these results indicate that natural Ab produced by peritoneal B cells binds within the glomerulus after renal I/R and contributes to functional renal injury. However, nonperitoneal B cells attenuate renal injury after I/R, possibly through the production of IL-10.

ischemia/reperfusion; kidney; complement activation; natural Ab

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Podaci o izdanju

185 (7)

2010.

4393-4400

objavljeno

0022-1767

10.4049/jimmunol.0903239

Povezanost rada

Temeljne medicinske znanosti

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