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Abstract
Anti-tRNA autoantibodies are associated with interstitial lung disease (ILD), in at least two clinical scenarios: the anti-synthetase syndrome (ASSD) and interstitial pneumonia with autoimmune features (IPAF). Under pathological conditions, cytokines indicate the participating elements and the course of inflammatory phenomena. We aimed to quantify serum concentrations of different inflammatory cytokines profiles in patients with anti-tRNA associated ILD (anti-tRNA-ILD) and estimate the association between these and ILD improvement and progression. Serum levels of 18 cytokines from baseline and after six months of treatment of ILD patients’ positives to anti-tRNA were included in the current study. At six months, patients were classified as with or without ILD progression. A total of 39 patients were included (10 anti-Jo1, eight anti-PL7, 11 anti-PL12, and 10 anti-Ej). Three patients (7.6%) had ILD progression (progressors patients, PP) and showed statistically higher levels in IL-4, IL-10, IL-17A, IL-22, GM-CSF, IL-1β, IL-6, IL-12, IL-18, and TNF-α, compared to patients without disease progression (no progressors patients, NPP). IL-17A, IL-1β, and IL-6 (T-helper-lymphocyte (Th)17 inflammatory cytokine profile) were elevated and had a high discriminatory capacity in distinguishing ILD PP of those NPP at follow-up. Overall, there is an association between the cytokines of the Th17 inflammatory profile and the ASSD progression.
Highlights
The anti-aminoacyl transfer-RNA-synthetases autoantibodies are diverse and include anti-EJ, anti-OJ, anti-PL7, anti-PL12, anti-SC, anti-KS, anti-JS, anti-Ha or anti-YRS, anti-tryptophanyl, and anti-Zo and anti-Jo1 [1], the latter being the most frequent
This study which was designed to evaluate the association between the cytokines’ concentrations and the pulmonary outcome of interstitial lung disease (ILD) patients positive to anti-tRNA autoantibodies, shows that the Th17 profile of immune response is associated with ILD progression
This report describes for the first time that the Th17 inflammatory profile could have a fundamental role in the pathophysiology of ILD associated with anti-tRNA and the possible role of the cytokines of the Th17 inflammatory profiles as biomarkers and therapeutic targets in anti-tRNA-ILD
Summary
The anti-aminoacyl transfer-RNA-synthetases (anti-tRNA) autoantibodies are diverse and include anti-EJ (anti-glycyl), anti-OJ (anti-isoleucyl), anti-PL7 (anti-threonyl), anti-PL12 (anti-alanyl), anti-SC (anti-lysil), anti-KS (anti-asparaginyl), anti-JS (anti-glutaminyl), anti-Ha or anti-YRS (anti-threonyl), anti-tryptophanyl, and anti-Zo (anti-phenylalanyl) and anti-Jo1 (anti-histidyl) [1], the latter being the most frequent. The anti-tRNA are associated to interstitial lung disease ILD (anti-tRNA-ILD) in at least two clinical scenarios: the antisynthetase syndrome (ASSD), an inflammatory myopathy (IM) characterized by arthritis, mechanic’s hands, fever, Raynaud’s phenomenon, and ILD [1], as well as interstitial pneumonia with autoimmune features (IPAF) [2] (a classification criterion for ILD patients and features of autoimmunity, but not definitive for established criteria of connective tissue disease) Both ASSD and IPAF positive to anti-tRNA share the same ILD high-resolution tomographic patterns (HRCT) and response to medical treatment [3,4], it seems that both clinical conditions are clinical variations of the same pathophysiological process. Some genetic background would favor the loss of self-tolerance, which would trigger an abnormal sensitization towards own cells and tissues turning a local event into a systemic disease following pathways, this is still poorly understood [7]
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