Systemic lupus erythematosus (SLE) is an autoimmune disease with unknown etiology. Periods of elevated disease activity, or SLE flares, cause significant organ damage, medication toxicity, and morbidity in patients. However, how a normally suppressed immune system mounts an aggressive autoimmune response that causes a flare is not known.
Our goal is to understand the mechanisms underlying the increase in autoimmune response and how cooperation between immune cells aggravates disease. Innate immune cells such as monocytes and neutrophils are the first cells to respond to infection or inflammatory events, and can therefore shape both a normal immune response to fight an infection as well as an autoimmune response. We utilize different approaches to understand the how these cells worsen the immune response in SLE. We aim to understand the role of a common viral infection on initiation of autoimmune response. We also study how this initial autoimmune response can influence the function newly generated immune cells, eventually cascading into an uncontrolled inflammatory response, which results in SLE flare.
Our studies will identify specific pathways that regulate flares and will lead to identification of new diagnostic markers as well as new targets for therapy.
B.Sc., Abasaheb Garware College, University of Pune, India, 1997
M.Sc., University of Pune, Pune, India, 1999
M.S., University of Louisville, Louisville, KY, 2003
Ph.D., University of Louisville, Louisville, KY, 2006
Postdoctoral Fellow, University of Pennsylvania, Philadelphia, PA, 2008
Joined OMRF Scientific Staff in 2019
Jog NR, Chakravarty EF, Guthridge JM, James JA. Epstein Barr Virus Interleukin 10 Suppresses Anti-inflammatory Phenotype in Human Monocytes. Front Immunol. 2018 Oct 9;9:2198. eCollection 2018. PMID: 30356670 PMCID: PMC6189329
Corradetti C, Jog NR, Cesaroni M, Madaio M, Caricchio R. Estrogen Receptor α Signaling Exacerbates Immune-Mediated Nephropathies through Alteration of Metabolic Activity. J Immunol. 2018 Jan 15;200(2):512-522. Epub 2017 Dec 13. PMID: 29237779 PMCID: PMC5760359
Jog NR, Frisoni L, Shi Q, Hernandez S, Monestier M, Craft J, Luning-Prak ET, Caricchio R. Caspase Activated DNase is Required to Maintain Tolerance to Lupus Nuclear Autoantigens. Arthritis Rheum. 2012 Apr;64(4):1247-56. Epub 2011 Nov 29. PMID: 22127758 PMCID: PMC3292632
Jog NR*, Blanco I*, Lee I, Putterman C, Caricchio R. Urinary High Mobility Group Box-1 Associates Specifically with Lupus Nephritis Class V. Lupus. 2016 Dec;25(14):1551-1557. Epub 2016 Apr 12. (*Equal contribution) PMID: 27075010 PMCID: PMC5061582
Jog NR, Dinnall JA, Gallucci S, Madaio MP, Caricchio R. Poly (ADP-Ribose) Polymerase-1 Regulates the Progression of Immune-mediated Nephritis by Inducing Necrotic Cell Death and Modulating Inflammatory Response in Males. J Immunol. 2009 Jun 1;182(11):7297-306. PMID: 19454727 PMCID: PMC4827346
Jog NR, Caricchio R. Differential regulation of Cell Death Programs in Males and Females by Poly (ADP-Ribose) Polymerase-1 and 17b Estradiol. Cell Death & Dis. 2013 Aug 8;4:e758. PMID: 23928697 PMCID: PMC3763428
Jog NR, Rane MJ, Lominadze G, Luerman GC, Ward RA, McLeish KR. The Actin Cytoskeleton Regulates Exocytosis of all Neutrophil Granule Subsets. Am J Physiol Cell Physiol. 2007 May; 292(5): C1690-700. Epub 2007, Jan 3. PMID: 17202227
Sriram U, Varghese L, Bennett HL, Jog NR, Shivers DK, Ning Y, Behrens EM, Caricchio R, Gallucci S. Myeloid Dendritic Cells from B6.NZM Sle1/Sle2/Sle3 Lupus-prone Mice express an Interferon Signature that Precedes Disease Onset. J Immunol. 2012 Jul 1;189(1):80-91. Epub 2012 Jun 1. PMID: 22661089 PMCID: PMC3381850
Arthritis & Clinical Immunology Research Program, MS 53
Oklahoma Medical Research Foundation
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