A photo of John Harley.

Director, Center for Autoimmune Genomics and Etiology (CAGE)

Professor, UC Department of Pediatrics


Board Certified

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Biography & Affiliation


Growing up, both of my parents were physicians. I remember being about 4 years old when I went with my dad on a house call in the middle of winter riding in the snowplow through deep snow to get there. So, I inherited a measure of tenacity.

I knew early in life that I wanted a career that would be important. After first studying physics in college, I decided that the life and death issues facing physicians would be more motivating. This realization led me to an MD-PhD program at the University of Pennsylvania.

During my MD-PhD training, before I had decided on a research focus, one of my best friends died. He had systemic lupus erythematosus and was being cared for by the best doctors in the country. I recall thinking that no one understood his disease and that maybe I could figure out its causes.

Despite all of the complexities and vagaries of life, I believe this quest — which is now more than four decades old — has been a success. Our group leads the effort to build the circumstantial evidence that systemic lupus erythematosus is actually caused by the Epstein-Barr virus. This virus causes most of mononucleosis cases and infects nearly all of us by the time we are adults.

The lessons that we are learning for lupus turn out to be crucial for a whole host of other diseases. If we are able to leverage our success with this one disease, then we can benefit the millions of people affected by many other serious and life-threatening conditions.

I am humbled and honored to hold the title of David Glass Endowed Chair in Pediatrics, which recognizes the work of a former Cincinnati Children’s Hospital Medical Center rheumatology division director. Dr. Glass was a serious scientist and a wonderful human being and friend. He gave the rest of us an extraordinary example of the intellectual life of a profoundly compassionate scholar.

Academic Affiliation

Professor, UC Department of Pediatrics



Blog Posts

‘Mono’ Virus Linked to Seven Serious Diseases

Autoimmune Disorders

‘Mono’ Virus Linked to Seven Serious Diseases

John B. Harley, MD, PhD, Leah C. Kottyan, PhD ...6/30/2019


A polygenic and phenotypic risk prediction for polycystic ovary syndrome evaluated by phenomewide association studies. Joo, YY; Actkins, K; Pacheco, JA; Basile, AO; Carroll, R; Crosslin, DR; Day, F; Denny, JC; Edwards, DR V; Hakonarson, H; et al. Journal of Clinical Endocrinology and Metabolism. 2020; 105:1918-1936.

CNV Association of Diverse Clinical Phenotypes from eMERGE reveals novel disease biology underlying cardiovascular disease. Glessner, JT; Li, J; Desai, A; Palmer, M; Kim, D; Lucas, AM; Chang, X; Connolly, JJ; Almogeura, B; Harley, JB; et al. International Journal of Cardiology. 2020; 298:107-113.

Epstein Barr virus nuclear antigen 1 (EBNA-1) peptides recognized by adult multiple sclerosis patient sera induce neurologic symptoms in a murine model. Jog, NR; McClain, MT; Heinlen, LD; Gross, T; Towner, R; Guthridge, JM; Axtell, RC; Pardo, G; Harley, JB; James, JA. Journal of Autoimmunity. 2020; 106:102332-102332.

GWAS and enrichment analyses of non-alcoholic fatty liver disease identify new trait-associated genes and pathways across eMERGE Network. Namjou, B; Lingren, T; Huang, Y; Parameswaran, S; Cobb, BL; Stanaway, IB; Connolly, JJ; Mentch, FD; Benoit, B; Niu, X; et al. BMC Medicine. 2019; 17.

Complete tracheal ring deformity a translational genomics approach to pathogenesis. Sinner, DI; Carey, B; Zgherea, D; Kaufman, KM; Leesman, L; Wood, RE; Rutter, MJ; de Alarcon, A; Elluru, RG; Harley, JB; et al. American Journal of Respiratory and Critical Care Medicine. 2019; 200:1267-1281.

Harmonizing Clinical Sequencing and Interpretation for the eMERGE III Network. Zouk, H; Venner, E; Muzny, DM; Lennon, NJ; Rehm, HL; Gibbs, RA; Walker, K; Gordon, AS; Bowser, M; Harden, MV; et al. The American Journal of Human Genetics. 2019; 105:588-605.

Association of Epstein-Barr virus serological reactivation with transitioning to systemic lupus erythematosus in at-risk individuals. Jog, NR; Young, KA; Munroe, ME; Harmon, MT; Guthridge, JM; Kelly, JA; Kamen, DL; Gilkeson, GS; Weisman, MH; Karp, DR; et al. Annals of the Rheumatic Diseases. 2019; 78:1235-1241.

Gender Differences in Demographic and Health Characteristics of the Million Veteran Program Cohort. Harrington, KM; Nguyen, XT; Song, RJ; Hannagan, K; Quaden, R; Gagnon, DR; Cho, K; Deen, JE; Muralidhar, S; O'Leary, TJ; et al. Women's Health Issues. 2019; 29 Suppl 1:S56-S66.

Amino acid signatures of HLA Class-I and II molecules are strongly associated with SLE susceptibility and autoantibody production in Eastern Asians. Molineros, JE; Looger, LL; Kim, K; Okada, Y; Terao, C; Sun, C; Zhou, XJ; Raj, P; Kochi, Y; Suzuki, A; et al. PLoS Genetics. 2019; 15:e1008092-e1008092.

Latent autoimmunity across disease-specific boundaries in at-risk first-degree relatives of SLE and RA patients. James, JA; Chen, H; Young, KA; Bemis, EA; Seifert, J; Bourn, RL; Deane, KD; Demoruelle, MK; Feser, M; O'Dell, JR; et al. EBioMedicine. 2019; 42:76-85.