Mitochondrial Dysfunction in the Liver and Antiphospholipid Antibody Production Precede Disease Onset and Respond to Rapamycin in Lupus-Prone Mice-Reference-Cited by-同舟云学术

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Mitochondrial Dysfunction in the Liver and Antiphospholipid Antibody Production Precede Disease Onset and Respond to Rapamycin in Lupus-Prone Mice

Published:2016-10-27 Issue:11 Volume:68 Page:2728-2739
ISSN:2326-5191
Container-title:Arthritis & Rheumatology
language:en
Short-container-title:Arthritis & Rheumatology

Author:

Oaks Zachary¹,Winans Thomas¹,Caza Tiffany¹,Fernandez David¹,Liu Yuxin¹,Landas Steve K.¹,Banki Katalin¹,Perl Andras¹

Affiliation:

1. State University of New York, Upstate Medical University; Syracuse

Funder

NIH (National Institute of Allergy and Infectious Diseases and National Institute of Diabetes and Digestive and Kidney Diseases)

Central New York Community Foundation

Publisher

Wiley

Subject

Immunology,Rheumatology,Immunology and Allergy

Reference49 articles.

1. Systemic lupus erythematosus;Tsokos;N Engl J Med,2011

2. Rapamycin reduces disease activity and normalizes T-cell activation-induced calcium fluxing in patients with systemic lupus erythematosus;Fernandez;Arthritis Rheum,2006

3. Activation of mammalian target of rapamycin controls the loss of TCRζ in lupus T cells through HRES-1/Rab4-regulated lysosomal degradation;Fernandez;J Immunol,2009

4. Mechanistic target of rapamycin activation triggers IL-4 production and necrotic death of double-negative T cells in patients with systemic lupus erythematosus;Lai;J Immunol,2013

5. HRES-1/RAB4-mediated depletion of Drp1 impairs mitochondrial homeostasis and represents a target for treatment in SLE;Caza;Ann Rheum Dis,2014

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