title: Biological and clinical effects of anti-TNFalpha treatment.
abstract: Tumor necrosis factor alpha (TNFalpha) is implicated in the pathogenesis of many chronic inflammatory diseases such as rheumatoid arthritis (RA), psoriasis and psoriatic arthritis (PsA), ankylosing spondylitis (AS), Crohn's disease, ulcerative colitis and uveitis. The availability of new pharmacological agents (infliximab, etanercept, adalimumab), able to selectively block the TNFalpha, has recently offered new opportunity for the treatment of these diseases. TNFalpha antagonists are different in the mechanism of action and are all effective agents in the treatment of RA and several chronic inflammatory diseases as a large number of controlled clinical trials have shown. Among biological effects of TNFalpha antagonists, the production of autoantibodies has been emphasized. This phenomenon is not correlated with the disease background, since anti-nuclear antibodies (ANA) and anti-double stranded-DNA antibodies (anti-dsDNA) induction is observed in RA as well as in spondyloarthritis (SpA) patients. Nonetheless, recent studies had reported a significant reduction in the serum titre of rheumatoid factor (RF) and/or anti-cyclic citrullinated peptide antibodies (anti-CCP) during anti-TNFalpha therapy. The TNFalpha antagonists represent a significant advance in the therapy of active RA and other chronic inflammatory diseases. However, they have distinct biological, clinical, and pharmacological properties that must be considered when selecting a drug for therapy.
authors.affiliation: Cattedra e UOC Reumatologia, Università di Roma La Sapienza, Policlinico Umberto I, 00161 Roma, Italy. Electronic address: guido.valesini@uniroma1.it.
authors.forename: G
authors.initials: G
authors.lastname: Valesini
authors.affiliation: Cattedra e UOC Reumatologia, Università di Roma La Sapienza, Policlinico Umberto I, 00161 Roma, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Iannuccelli
authors.affiliation: Cattedra e UOC Reumatologia, Università di Roma La Sapienza, Policlinico Umberto I, 00161 Roma, Italy.
authors.forename: E
authors.initials: E
authors.lastname: Marocchi
authors.affiliation: Cattedra e UOC Reumatologia, Università di Roma La Sapienza, Policlinico Umberto I, 00161 Roma, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Pascoli
authors.affiliation: Cattedra e UOC Reumatologia, Università di Roma La Sapienza, Policlinico Umberto I, 00161 Roma, Italy.
authors.forename: V
authors.initials: V
authors.lastname: Scalzi
authors.affiliation: Cattedra e UOC Reumatologia, Università di Roma La Sapienza, Policlinico Umberto I, 00161 Roma, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Di Franco
mesh_terms: D000068879:Adalimumab; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000276:immunology / Q000494:pharmacology / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000276:immunology; D001323:Autoantibodies / Q000096:biosynthesis / Q000097:blood; D002908:Chronic Disease; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology / Q000494:pharmacology / Q000627:therapeutic use; D007249:Inflammation / Q000188:drug therapy* / Q000276:immunology; D000069285:Infliximab; D018124:Receptors, Tumor Necrosis Factor / Q000276:immunology / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000276:immunology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D001323:Autoantibodies; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept