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We read with interest the study by Neerinckx et al1 addressing the expression of interleukin (IL)-23p19 and of autophagy genes in the synovium and in the peripheral blood mononuclear cells of patients with ankylosing spondylitis (AS). Differently from our observation in the gut,2 the authors failed to demonstrate any significant increase by RT-PCR in the expression of synovium autophagy-related genes (ATG16L1, IRGM, MAP1LC3A, ATG5, HSPA8 and HSP90AA1) together with no significant overexpression of IL-23p19 compared with disease and healthy controls.
We have previously demonstrated by immunohistochemistry that in the …
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