Autoimmune-like syndromes during TNF blockade: does infection have a role?

• Published in: Nature reviews. Rheumatology Vol. 7; no. 7; pp. 429 - 434
• Main Author: Prinz, Joerg C
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.07.2011; Nature Publishing Group
• Subjects: 631/250/254; 692/699/249/1313; 692/700/565/2194; 692/700/565/251; Antagonists; Arthritis; Autoimmune diseases; Autoimmune Diseases - immunology; Autoimmune Diseases - metabolism; Autoimmune Diseases - pathology; Autoimmunity; Bacterial infections; Biomarkers - metabolism; Care and treatment; Cytotoxicity; Demyelination; Development and progression; Diagnosis; Disease; Humans; Immunological tolerance; Infection; Infection - immunology; Infection - metabolism; Infection - pathology; Infections; Inflammatory diseases; Lupus; Medical laboratories; Medicine; Medicine & Public Health; Monoclonal antibodies; Nervous system; opinion-2; Peripheral neuropathy; Physiological aspects; Rheumatology; Risk factors; Sclerosis; Syndrome; Systemic lupus erythematosus; Tumor necrosis factor; Tumor Necrosis Factor-alpha - antagonists & inhibitors; Tumor Necrosis Factor-alpha - metabolism; Tumor necrosis factor-TNF; Viral infections; Germany
• ISSN: 1759-4790; 1759-4804
• DOI: 10.1038/nrrheum.2011.35

Autoimmune-like syndromes (AILS), such as lupus-like syndrome and inflammatory neuropathies, are occasionally seen in patients treated with tumor necrosis factor (TNF) antagonists, although the pathogenetic mechanisms underlying these syndromes are not well understood. In this article, the author suggests that infections might trigger, amplify or mimic AILS in patients receiving anti-TNF therapy. Tumor necrosis factor (TNF) antagonists are effective treatments for immune-mediated inflammatory disorders. The most dreaded adverse events associated with these agents are severe infections. Occasionally, patients develop autoimmune-like syndromes (AILS), which include episodes of lupus-like syndrome, multiple-sclerosis-like demyelination and inflammatory neuropathies. The underlying pathologic mechanisms of these syndromes remain, however, matters of debate. Evidence indicates that the onset of systemic lupus erythematosus, inflammatory nervous system demyelination or peripheral neuropathies in the general population may have infectious etiologies. This article discusses whether infectious agents might also have a role in the development of AILS during anti-TNF therapy. TNF antagonists might facilitate the dissemination of dormant or newly acquired viral or bacterial infections, which either directly promote symptoms that mimic autoimmune diseases or break immunological tolerance and induce autoimmunity in predisposed individuals. The occurrence of AILS during TNF blockade should, therefore, lead to reliable infection screening strategies to identify infection-induced autoimmunity and autoimmune mimics.