Home |
Current Issue |
Past Issues |
In the Clinic |
ACP Journal Club |
CME |
Collections |
Audio/Video |
Mobile |
Subscribe |
Tools |
Help |
ACP Online
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
18 June 2002 | Volume 136 Issue 12 | Pages 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.
Author and Article Information
From Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania.
Acknowledgments: The authors thank Drs. John Abruzzo, Pam Norton, Andrew Koenig, and Stacy Fitch for their careful review and helpful suggestions in the preparation of this manuscript.
Grant Support: By the Mona Schneidman Foundation.
Requests for Single Reprints: J. Bruce Smith, MD, Jefferson Medical College, 613 Curtis Building, Philadelphia, PA 19107.
Current Author Addresses: Dr. Smith: Jefferson Medical College, 1015 Walnut Street, Suite 613Curtis Building, Philadelphia, PA 19107.
Dr. Haynes: Jefferson Medical College, 1015 Walnut Street, Philadelphia, PA 19107. REVIEW
Rheumatoid ArthritisA Molecular Understanding
![]()
This article has been cited by other articles:
![]() |
J. M. Hansen, H. Zhang, and D. P. Jones Mitochondrial Thioredoxin-2 Has a Key Role in Determining Tumor Necrosis Factor-{alpha}-Induced Reactive Oxygen Species Generation, NF-{kappa}B Activation, and Apoptosis Toxicol. Sci., June 1, 2006; 91(2): 643 - 650. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. C. Huber, O. Distler, I. Tarner, R. E. Gay, S. Gay, and T. Pap Synovial fibroblasts: key players in rheumatoid arthritis Rheumatology, June 1, 2006; 45(6): 669 - 675. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Doan and E. Massarotti Rheumatoid Arthritis: An Overview of New and Emerging Therapies J. Clin. Pharmacol., July 1, 2005; 45(7): 751 - 762. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Karlsson, M. Johannesson, T. Lindvall, P. Wernhoff, R. Holmdahl, and A. Andersson Genetic Interactions in Eae2 Control Collagen-Induced Arthritis and the CD4+/CD8+ T Cell Ratio J. Immunol., January 1, 2005; 174(1): 533 - 541. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Gause Progress in the treatment of rheumatic disease Nephrol. Dial. Transplant., January 1, 2003; 18(1): 13 - 16. [Full Text] [PDF] |
||||