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07/19/04

Scientific and clinical aspects of the management of immune-mediated inflammatory disorders (I.M.I.D.)



Overexpression of pleiotropic cytokines stimulates many I.M.I.D

Montréal, Canada — July 20, 2004 — Earlier diagnosis and more aggressive treatment of Immune-Mediated Inflammatory Disorders (I.M.I.D.), such as rheumatoid arthritis, multiple sclerosis and Crohn's disease, may offer the opportunity to prevent some of the more severe manifestations, as well as the progression of these diseases.

Overexpression of interleukin-12 (IL-12) and interleukin-23 (IL-23), which share a common p40 receptor, may be significant to the progression of a number of significant diseases such as multiple sclerosis, Crohn's disease, and psoriasis. In addition, the pro-inflammatory and immuno-stimulatory cytokine IL-6 may have crucial impact in rheumatoid arthritis and lupus as well as some cardiovascular and metabolic disorders, according to recent immunologic data.

"The IL-12 family of cytokines plays an important role in bridging both innate and adaptive immune responses," says Scott Plevy, MD. "It is therefore not surprising that deregulation of IL-12 function could contribute to the pathophysiology of I.M.I.D." Dr. Plevy is an associate professor of medicine and immunology at the University of Pittsburgh School of Medicine in Pittsburgh, Pennsylvania. He has extensive clinical and research experience related to inflammatory bowel disorders.

The role of tumor necrosis factor alfa (TNF-alpha) in stimulating I.M.I.D. is already widely recognized. According to Albert Lasker Clinical Medical Research Award winner Professor Marc Feldmann, MD, PhD, "Induction of tumor necrosis factor influences many biological effects that are related to a wide range of Immune-Mediated Inflammatory Disorders, including rheumatoid arthritis, psoriasis, Crohn's disease, and numerous other life-limiting diseases. By blocking the effects of TNF, we are learning how to treat a number of I.M.I.D., and our increasing knowledge is allowing us to gain a greater appreciation of the way these diseases can be recognized and potentially managed in the future. Most importantly, TNF blockade can protect from tissue damage and promote healing of joints in rheumatoid arthritis and of fistulas in Crohn's disease."

Feldmann is professor and head of the Kennedy Institute of Rheumatology Division, Imperial College London and head of the Institute's Cytokine Biology and Cellular Immunology Group.

The term I.M.I.D. refers to a group of biologically interconnected diseases that share common inflammatory pathways and are characterized by immune dysregulation that results in acute or chronic inflammation, causing injury to the body. I.M.I.D. includes disorders as diverse as autoimmune conditions, some forms of cancer, some infectious diseases, and a variety of other chronic conditions that are the consequence of inflammation of selected tissues. While these diseases may appear very different, they may be caused by dysfunction in similar physiologic pathways.

Collectively, I.M.I.D. may affect between 5% and 7% of the western world's population, and as many as one in four patients admitted to hospitals in the U.S. suffers from an I.M.I.D. By identifying the molecular targets that trigger these disorders and developing new pharmaceutical and biopharmaceutical therapies, it should be possible to improve the lives of the patients most severely affected.

The Federation of Clinical Immunology Societies (FOCIS), an international "think tank" in clinical immunology, has designated funds and expertise to selected medical and clinical research centers to explore diseases of immune dysregulation from a basic research, translational research, and clinical science perspective. The FOCIS Centers of Excellence are organized to intensify and accelerate multidisciplinary scientific and clinical innovation, education, and advocacy in the field of clinical immunology. This concept encourages the opportunity for specialists in a variety of fields (gastroenterology, rheumatology, immunology, and other areas of specialty) to collaborate in seeking to advance our understanding of the underlying relationship among their disparate diseases, and to correlate that information with practical guidance on the management of these devastating diseases.

Plevy and Feldmann, together with Mercedes Rincón, PhD (University of Vermont, College of Medicine, Burlington, VT) will speak at a special session on "Pleiotropic Cytokines in Immune-Mediated Inflammatory Disorders: From the Bedside to the Bench," held on July 21, 2004 during the 12th International Congress of Immunology and the 4th Annual Conference of the Federation of Clinical Immunology Societies (FOCIS) in Montreal, Canada. The educational session is co-sponsored by FOCIS and McGill University, and is supported by an educational grant from Centocor, Inc.

Source: Eurekalert & others

Last reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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