A photo of Alexei Grom.

Research Director, Division of Rheumatology

Professor, UC Department of Pediatrics

513-636-3339

513-636-3328

Board Certified

My Biography & Research

Biography

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

Departments

Rheumatology, Lupus, Rheumatology

Science Blog

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

Serum S100A8/A9 and S100A12 Levels in Children With Polyarticular Forms of Juvenile Idiopathic Arthritis: Relationship to Maintenance of Clinically Inactive Disease During Anti-Tumor Necrosis Factor Therapy and Occurrence of Disease Flare After Discontinuation of Therapy. Hinze, CH; Foell, D; Johnson, AL; Spalding, SJ; Gottlieb, BS; Morris, PW; Kimura, Y; Onel, K; Li, SC; Grom, AA; et al. Arthritis and Rheumatology. 2019; 71:451-459.

A Multiparameter Flow Cytometry Analysis Panel to Assess CD163 mRNA and Protein in Monocyte and Macrophage Populations in Hyperinflammatory Diseases. Thornton, S; Tan, R; Sproles, A; Do, T; Schick, J; Grom, AA; DeLay, M; Schulert, GS. Journal of immunology (Baltimore, Md. : 1950). 2019; 202:1635-1643.

Neutrophils From Children With Systemic Juvenile Idiopathic Arthritis Exhibit Persistent Proinflammatory Activation Despite Long-Standing Clinically Inactive Disease. Brown, RA; Henderlight, M; Do, T; Yasin, S; Grom, AA; Delay, M; Thornton, S; Schulert, GS. Frontiers in Immunology. 2018; 9.

Risk, Timing, and Predictors of Disease Flare After Discontinuation of Anti-Tumor Necrosis Factor Therapy in Children With Polyarticular Forms of Juvenile Idiopathic Arthritis With Clinically Inactive Disease. Lovell, DJ; Johnson, AL; Huang, B; Gottlieb, BS; Morris, PW; Kimura, Y; Onel, K; Li, SC; Grom, AA; Taylor, J; et al. Arthritis and Rheumatology. 2018; 70:1508-1518.

Identification of enhanced IFN-gamma signaling in polyarticular juvenile idiopathic arthritis with mass cytometry. Throm, AA; Moncrieffe, H; Orandi, AB; Pingel, JT; Geurs, TL; Miller, HL; Daugherty, AL; Malkova, ON; Lovell, DJ; Thompson, SD; et al. JCI insight. 2018; 3.

Cat-Scratch Disease, a Diagnostic Consideration for Chronic Recurrent Multifocal Osteomyelitis. Harry, O; Schulert, GS; Frenck, RW; Shapiro, AH; Woltmann, JL; Smith, JA; Grom, AA. Journal of Clinical Rheumatology: practical reports on rheumatic and musculoskeletal disease. 2018; 24:287-290.

IL1RN Variation Influences Both Disease Susceptibility and Response to Recombinant Human Interleukin-1 Receptor Antagonist Therapy in Systemic Juvenile Idiopathic Arthritis. Arthur, VL; Shuldiner, E; Remmers, EF; Hinks, A; Grom, AA; Foell, D; Martini, A; Gattorno, M; Ozen, S; Prahalad, S; et al. Arthritis and Rheumatology. 2018; 70:1319-1330.

Cat-Scratch Disease, a Diagnostic Consideration for Chronic Recurrent Multifocal Osteomyelitis. Harry, O; Schulert, GS; Jr, FR W; Shapiro, AH; Woltmann, JL; Smith, JA; Grom, AA. Journal of Clinical Rheumatology: practical reports on rheumatic and musculoskeletal disease. 2018; 24:287-290.

Novel UNC13D Intronic Variant Disrupting an NF-kappa B Enhancer in a Patient With Recurrent Macrophage Activation Syndrome and Systemic Juvenile Idiopathic Arthritis. Schulert, GS; Zhang, M; Husami, A; Fall, N; Brunner, H; Zhang, K; Cron, RQ; Grom, AA. Arthritis and Rheumatology. 2018; 70:963-970.

Neutralization of IFN-gamma reverts clinical and laboratory features in a mouse model of macrophage activation syndrome. Prencipe, G; Caiello, I; Pascarella, A; Grom, AA; Bracaglia, C; Chatel, L; Ferlin, WG; Marasco, E; Strippoli, R; de Min, C; et al. Journal of Allergy and Clinical Immunology. 2018; 141:1439-1449.