J. Bruce Smith, MD; Mark K. Haynes, PhD
Smith JB, Haynes MK. Rheumatoid Arthritis—A Molecular Understanding. Ann Intern Med. 2002;136:908-922. doi: 10.7326/0003-4819-136-12-200206180-00012
Download citation file:
Published: Ann Intern Med. 2002;136(12):908-922.
The application of molecular immunology techniques in the study of rheumatoid arthritis has resulted in an explosion of knowledge on the risk factors for the disease, predictors of disease severity, the molecular mechanisms of inflammatory responses, and mechanisms of tissue destruction. We know, for example, that inheriting certain genes in the major histocompatibility complex partly dictates susceptibility and severity of rheumatoid arthritis. These genes and others in the major histocompatibility complex are critical for the occurrence of immune responses both constructive (prevention of infection, surveillance for malignant cells) and destructive (development of autoimmune diseases). We also now understand mechanisms of cell communication, regulation of immune responses, how the cells that mediate immune responses and tissue injury accumulate in tissues, and how the injury occurs. The knowledge itself is satisfying, but more important, based on this knowledge, effective and reasonably safe treatments that address basic mechanisms of the disease process have been developed and are now widely used. In fact, the newer treatments represent the “tip of the iceberg,” and as our basic knowledge increases, so too will the armamentarium with which we can fight rheumatoid arthritis and other similar autoimmune diseases.
For definitions of terms, see Glossary at end of text.
Learn more about subscription options.
Register Now for a free account.
Rheumatology, Rheumatoid Arthritis.
Results provided by:
Copyright © 2016 American College of Physicians. All Rights Reserved.
Print ISSN: 0003-4819 | Online ISSN: 1539-3704
Conditions of Use
This PDF is available to Subscribers Only