Different effects of global osteopontin and macrophage osteopontin in glomerular injury.
Trostel, Jessica; Truong, Luan D; Roncal-Jimenez, Carlos; Miyazaki, Makoto; Miyazaki-Anzai, Shinobu; Kuwabara, Masanari; McMahan, Rachel; Andres-Hernando, Ana; Sato, Yuka; Jensen, Thomas; Lanaspa, Miguel A; Johnson, Richard J; Garcia, Gabriela E.
Am J Physiol Renal Physiol
; 315(4): F759-F768, 2018 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-29717936
Macrophage A2A Adenosine Receptors Are Essential to Protect from Progressive Kidney Injury.
Absence of the lysosomal protein Limp-2 attenuates renal injury in crescentic glomerulonephritis.
Pattern recognition and renal defence in crescentic glomerulonephritis.
Absence of nicotinic acetylcholine receptor α7 subunit amplifies inflammation and accelerates onset of fibrosis: an inflammatory kidney model.
Transfusion of CD206<sup>+</sup> M2 Macrophages Ameliorates Antibody-Mediated Glomerulonephritis in Mice.
B-cell-derived IL-10 does not vitally contribute to the clinical course of glomerulonephritis.
Exacerbation of spontaneous autoimmune nephritis following regulatory T cell depletion in B cell lymphoma 2-interacting mediator knock-out mice.
Adenosine A(2A) receptor activation prevents progressive kidney fibrosis in a model of immune-associated chronic inflammation.
[Relationship between podocyte injury and macrophage infiltration in renal tissues of patients with lupus nephritis].
Monocytes Promote Crescent Formation in Anti-Myeloperoxidase Antibody-Induced Glomerulonephritis.