The steady advances in the diagnosis and treatment of rheumatic diseases and the impact on clinical practice originate in part from the research enterprise supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and other components of the National Institutes of Health (NIH). NIAMS’ programs in arthritis and rheumatic diseases cover the spectrum of basic, translational, and clinical research in a number of autoimmune and arthritis-related chronic diseases.
NIAMS and the other NIH institutes and centers are very fortunate to have the continued support of the Congress and the trust of the American public. To honor that trust, we are dedicated to conducting and supporting the best research in the most promising areas of science.
Intramural Research Program Explores the Boundaries of Rheumatic Diseases
The majority of NIAMS’ funding goes to support grants for investigators around the country and throughout the world. NIAMS also conducts research through its Intramural Research Program (IRP) on the NIH campus in Bethesda, Md.
Basic research is the backbone of NIH’s mission to acquire new knowledge to help prevent, detect, diagnose, and treat disease and disability. The IRP portfolio of basic and clinical research in rheumatology includes the study of immunity, autoimmunity, immune cell biology, and molecular immunology and inflammation. In the past few years, NIAMS investigators have made significant discoveries in the fields of autoimmunity and autoinflammatory diseases and immunodeficiency disorders.
NIAMS investigator Richard Siegel, MD, PhD, and colleagues found a potential new way to block inflammation in autoimmune diseases using a new target—a cell-surface receptor called DR3.1 Their research in mice suggests that blocking this receptor could slow or stop the damaging inflammation characteristic of autoimmune diseases, potentially without leaving the body vulnerable to serious infections, as many current therapies do.
In a study published in Nature, NIAMS Scientific Director John O’Shea, MD, and colleagues from the National Institute of Allergy and Infectious Diseases (NIAID) identified missing components in immune regulation in Job’s syndrome, a rare immunodeficiency disorder characterized by recurrent bacterial and fungal infections and bone and connective tissue abnormalities.2 They showed that Job’s sufferers lack a specific type of infection-fighting white blood cell called Th17, making them vulnerable to attacks by bacteria and fungi.
NIAMS senior investigator Juan Rivera, PhD, O’Shea, and colleagues recently showed that the protein Lyn kinase, expressed in basophils, helps control the way T helper cells differentiate in mice.3 This ability to govern cell differentiation makes basophils and their cell-signaling pathways possible targets for future therapeutic strategies in immune-mediated diseases.
