IL-34–Dependent Intrarenal and Systemic Mechanisms Promote Lupus Nephritis in MRL-Faslpr Mice | Zendy

Yukihiro Wada | Zendy; Hilda M. González-Sánchez | Zendy; Julia WeinmannMenke | Zendy; Yasunori Iwata | Zendy; Amrendra K. Ajay | Zendy; Myriam Meineck | Zendy; Vicki Rubin Kelley | Zendy

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IL-34–Dependent Intrarenal and Systemic Mechanisms Promote Lupus Nephritis in MRL-Faslpr Mice

Author(s) -

Yukihiro Wada,

Hilda M. González-Sánchez,

Julia WeinmannMenke,

Yasunori Iwata,

Amrendra K. Ajay,

Myriam Meineck,

Vicki Rubin Kelley

Publication year - 2019

Publication title -

journal of the american society of nephrology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 4.451

H-Index - 279

eISSN - 1533-3450

pISSN - 1046-6673

DOI - 10.1681/asn.2018090901

Subject(s) - lupus nephritis , systemic lupus erythematosus , nephritis , autoantibody , medicine , immunology , kidney , glomerulonephritis , disease , antibody

In people with SLE and in the MRL- Fas lpr lupus mouse model, macrophages and autoantibodies are central to lupus nephritis. IL-34 mediates macrophage survival and proliferation, is expressed by tubular epithelial cells (TECs), and binds to the cFMS receptor on macrophages and to a newly identified second receptor, PTPRZ.

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