Unmet needs in the treatment of autoimmunity: from aspirin to stem cells.
As rheumatologic diseases became understood to be autoimmune in nature, the drugs used to treat this group of conditions has evolved from herbal or plant derived anti-inflammatory agents, such as salicylates, quinine and colchicine to the many recently approved biological response modifiers. These new drugs, especially the anti-tumor necrosis factor agents, have shown remarkable efficacy in autoimmune diseases, and there are new agents under investigation that will provide additional treatment options. In between, the world was introduced to cortisone and all of its derivatives, as chemical synthesis led to better, more efficacious drugs with lesser side effects. Disease modifying anti-rheumatic agents have actually been around since the first half of the 20th century, but only began to be used in the treatment of autoimmune diseases in the 1970s and 1980s. One advantage is that they have been invaluable in their ability to offer "steroid sparing" to decrease the adverse effects of steroids. Research over the past decade has resulted in a new class of drugs that influence cytokine regulatory pathways such as the Janus associated kinase inhibitors. The promise of personalized medicine now permeates current research into new pharmacological agents for the treatment of autoimmune disease. The new appreciation for the gene-environment interaction in the pathogenesis of most diseases especially those as heterogeneous as autoimmune diseases, has led to our focus on targeted therapies. Add to that the new knowledge of epigenetics and how changes in DNA and histone structure affect expression of genes that can play a role in immune signaling, and we now have a new exciting frontier for cutting edge drug development. The history of treatment of autoimmune diseases is really only a little over a century, but so much has changed, leading to increasing lifespans and improved quality of life of those who suffer from these ailments.
Division of Allergy and Immunology, Thomas Jefferson University, Nemours/A.I. duPont Hospital for Children, 1600 Rockland Road, Wilmington, DE 19803, USA. Electronic address: cchang@nemours.org.
Christopher
C
Chang
D000818:Animals; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use*; D001327:Autoimmune Diseases / Q000628:therapy*; D015551:Autoimmunity; D023281:Genomics; D006801:Humans; D013234:Stem Cells
D018501:Antirheumatic Agents; D001241:Aspirin
Biological response modifiers; DMARDS; Glucocorticoids; Janus associated kinase inhibitors; Rheumatoid arthritis; Systemic lupus erythematosus