Immunology Faculty Member - Peter Nigrovic, MD

Peter Nigrovic, MD

Brigham and Women's Hospital
Div. of Rheum, Imm and Allergy
One Jimmy Fund Way, SMith 516B
Boston, MA 02115
Tel: 617-525-1010

The Nigrovic lab studies basic immune mechanisms of inflammatory arthritis in adults and children. This work employs both murine models (e.g. K/BxN, IL-1ra-/-) and human specimens. Active projects include:

1) Innate mechanisms of inflammatory synovitis. Our group helped to identify a role for the mast cell in the initiation of murine synovitis. We are interested in the contribution of this lineage to chronic arthritis; in mechanisms that underlie the expansion of these cells in inflamed synovial tissue; and in understanding when mast cells are required and when they are dispensable. These latter studies have led to new insights in the role of neutrophils, platelets and megakaryocytes in inflammatory arthritis. Current fellows have projects focusing on the role of Ly6G family members (Ly6G, CD177) in neutrophil migration; on myeloid development; and on megakaryocyte biology.

2) IgG glycosylation. In murine and human arthritis, IgG can be the primary driver of joint inflammation. The ability of IgG to engage Fc receptors and complement is dependent upon two specific glycans within the Fc region. The distribution of these glycoforms changes in inflammatory arthritis, as well as with age and gender. We are interested in mechanisms underlying these changes and their relevance for immune function and disease pathogenesis.

3) T cell-mediated immunological memory in the joint.
Clinical observations suggest that patients with arthritis respond better to treatment early rather than late, and that the pattern of joints affected in an individual patient is remarkably stable, even as disease runs a course over many decades. We are interested in changes that occur in T cell phenotype and repertoire that may drive these clinical phenomena.

4) Genetic insights into arthritis pathogenesis. We have recently developed several novel molecular tools that help to bridge the gap between genome wide association studies (GWAS) and molecular pathways relevant to disease. We are beginning to apply these tools to rheumatoid arthritis and to juvenile idiopathic arthritis in order to use human genetics to identify pathogenic mechanisms.

Clinically, Dr. Nigrovic is a pediatric and adult rheumatologist and directs the Center for Adults with Pediatric Rheumatic Illness (CAPRI) at the Brigham and Women’s Hospital. He directs arthritis biorepositories at Boston Children’s Hospital and at the Brigham and Women’s Hospital. He is an associate editor at
Arthritis & Rheumatology and chairs the Translational Research and Technology Committee of the US/Canadian pediatric rheumatology research group CARRA.

Last Update: 1/5/2015


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