A photo of Alexei Grom.

Research Director, Division of Rheumatology

Professor, UC Department of Pediatrics



Board Certified

My Biography & Research


The research of Alexei Grom, MD, has mainly involved two translational projects focused on two autoimmune diseases – systemic juvenile rheumatoid arthritis and juvenile dermatomyositis. In both projects, recent advances of cellular immunology are applied to these diseases to promote better understanding of their pathogenesis and treatment.

Systemic onset juvenile rheumatoid arthritis and an associated condition known as macrophage activation syndrome are severe and often devastating illnesses. The pathological mechanisms are not known but Dr. Alexei Grom has focused his research on NK and cytotoxic cell function in this disease. The rationale for this approach has been based on the strong clinical similarities between MAS and the better understood autosomal recessive disorder familial hemophagocytic lymphohistiocytosis, in which the uncontrolled proliferation of T cells and macrophages has been recently associated with decreased NK cell and cytotoxic cell functions secondary to mutations in the gene encoding perforin. Recent observations suggest as in FHLH, MAS patients also have profoundly depressed NK function. Moreover, a large subgroup of systemic JRA patients has very similar immunologic abnormalities. Combined with the evidence of the immunoregulatory role of NK cells in many immune responses, this suggests that NK dysfunction is relevant to the pathogenesis of MAS. New directions have thus been established for research in this poorly understood disease.

Juvenile dermatomyositis is a chronic inflammatory condition involving primarily muscles and skin. The most characteristic feature of JDM is vascular damage associated with the capillary necrosis that eventually leads to capillary loss and tissue ischemia. The project is based on the hypothesis that capillary loss in this condition may be caused by angiostatic chemokines that are prominent in the inflammatory response in the affected muscles.

Additional Languages

French, Russian

Academic Affiliation

Professor, UC Department of Pediatrics


Rheumatology, Rheumatology, Lupus Center

My Locations

My Education

MD: Leningrad (St. Petersburg) Pediatric Medical Institute, Russia, 1986.

Residency: Leningrad (St. Petersburg) Medical Institute, Russia, 1988; Children's Hospital Medical Center, Cincinnati, OH, 1998.

Fellowship: Leningrad (St. Petersburg) Pediatric Medical Institute, Russia, 1991; Children's Hospital Medical Center, Cincinnati, OH, 1995.

Certification: Pediatrics, 1999.

My Publications

Schulert G, Fall N, Harley J, Shen N, Lovell DJ, Thornton S, Grom AA. Monocyte microRNA expression in active systemic juvenile idiopathic arthritis reveals essential role of miR-125a-5p in polarized monocyte phenotypes. Arthritis Rheumatol. 2016.

Ravelli A, Minoia F, Davì S, Horne A, Bovis F, Pistorio A, Aricò M, Avcin T, Behrens EM, De Benedetti F, Filipovic L, Grom AA, Henter JI, Ilowite NT, Jordan MB, Khubchandani R, Kitoh T, Lehmberg K, Lovell DJ, Miettunen P, Nichols KE, Ozen S, Pachlopnik Schmid J, Ramanan AV, Russo R, Schneider R, Sterba G, Uziel Y, Wallace C, Wouters C, Wulffraat N, Demirkaya E, Brunner HI, Martini A, Ruperto N, Cron RQ. 2016 Classification Criteria for Macrophage Activation Syndrome Complicating Systemic Juvenile Idiopathic Arthritis: A European League Against Rheumatism/ American College of Rheumatology/ Paediatric Rheumatology International Trials Organisation Collaborative Initiative. Ann Rheum Dis. 2016;75:481-9.

Grom AA, Horne AC, De Benedetti F. Macrophage activation syndrome in the era of biologic therapy: clues to pathogenesis and impact on diagnostic approaches. Nature Rev Rheumatol. 2016.

Bracaglia C, Kathy de Graaf K, Marafon DP, D’Ario G, Guilhot F, Ferlin W, Prencipe G, Caiello I, Davì D, Schulert G, Ravelli A, Grom AA, De Benedetti F. Elevated circulating levels of interferon-γ and interferon- induced chemokines characterize patients with macrophage activation syndrome complicating systemic JIA. Ann Rheum Dis. 2016.

Schulert GS, Zhang, M, Fall N, Husami A, Kissell D, Hanosh A, Zhang K, Davis K, Jentzen JM, Siddiqui J, Smith LB, Harms PW, Grom AA, Cron RQ. Whole exome sequencing reveals mutations in hemophagocytic lymphohistiocytosis linked genes among fatal cases of H1N1 infection. J Infect Dis. 2016.

Grom AA, Ilowite N, Brunner HI, Ruperto N, Martinin A, Lovell D, Pascual V, Lheritier K, Abrams K. Canakinumab in Systemic Juvenile Idiopathic Arthritis: Impact on the Rate and Clinical Presentation of Macrophage Activation Syndrome. Arthritis Rheumatol. 2016;68:218-28.

Zhang M, Bemrich-Stolz CJ, Beukelman T, Dimmitt RA, Chatham WW, Zhang K, Li H, Grom AA, Cron RQ. A single copy RAB27a mutation leading to decreased NK cell cytolytic function and hemophagocytic lymphohistiocytosis. J Immunol. 2016;196(6):2492-503.

Schulert GS, Bobe K, McMasters R, Campbell K, Leslie N, Grom AA. Mevalonate kinase deficiency associated with recurrent liver dysfunction, macrophage activation syndrome and perforin gene polymorphism. Arthritis Care Res. 2015;67:1173-9.

Canna SW, Almeida de Jesus A, Gouni S, Brooks SR, Marrero B, Liu Y, Dimattia M, Zaal KJM, Montealegre-Sanchez G, Kim H, Chapelle D, Plass N, Huang Y, Biancotto A, Fleisher TA, J Duncan A, O’Shea JJ, Benseler S, Grom AA, Laxer RM, Goldbach-Mansky R. An activating NLRC4 inflammasome mutation causes a novel autoinflammatory syndrome presenting with recurrent Macrophage Activation Syndrome. Nature Genetics. 2014;46:1140-6.

Kaufman KM, Linghu B, Szustakowski JD, Husami A, Yang F, Zhang K, Filipovich A, Fall N, Harley JB, Nirmala NR, Grom AA. Whole Exome Sequencing Reveals Overlap Between Macrophage Activation Syndrome in Systemic Juvenile Idiopathic Arthritis and Familial Hemophagocytic Lymphohistiocytosis. Arthritis & Rheum. 2014;66:3486-95.