Abstract
Regulatory T cells (Tregs) are believed to be dysfunctional in autoimmunity. Juvenile idiopathic arthritis (JIA) and juvenile dermatomyositis (JDM) result from a loss of normal immune regulation in specific tissues such as joints or muscle and skin, respectively. Here, we discuss recent findings in regard to Treg biology in oligo-/polyarticular JIA and JDM, as well as what we can learn about Treg-related disease mechanism, treatment and biomarkers in JIA/JDM from studies of other diseases. We explore the potential use of Treg immunoregulatory markers and gene signatures as biomarkers for disease course and/or treatment success. Further, we discuss how Tregs are affected by several treatment strategies already employed in the therapy of JIA and JDM and by alternative immunotherapies such as anti-cytokine or co-receptor targeting. Finally, we review recent successes in using Tregs as a treatment target with low-dose IL-2 or cellular immunotherapy. Thus, this mini review will highlight our current understanding and identify open questions in regard to Treg biology, and how recent findings may advance biomarkers and new therapies for JIA and JDM.
Highlights
CD4+FOXP3+ regulatory T cells (Tregs) are a subset of CD4+ T helper cells present in lymphoid and non-lymphoid tissues, and are crucial for mediating tolerance to self, preventing allergies and controlling immune reactions after infections [1]
We discuss recent advances in the understanding of Treg biology in oligo-/ polyarticular juvenile idiopathic arthritis (JIA) and juvenile dermatomyositis (JDM), and what we can learn about Treg-related disease mechanisms, treatments and biomarkers from other diseases
It is clear that Tregs present challenges and opportunities in JIA and JDM research and clinical management (Figure 2)
Summary
CD4+FOXP3+ regulatory T cells (Tregs) are a subset of CD4+ T helper cells present in lymphoid and non-lymphoid tissues, and are crucial for mediating tolerance to self, preventing allergies and controlling immune reactions after infections [1]. They develop in the thymus or are induced in the periphery and exhibit contact-dependent and -independent mechanisms of action [1]. JDM is characterized by inflammation of muscles and skin, resulting in muscle weakness and rashes [reviewed in [5]] For both conditions researchers may take advantage of clinical sample collection from the site of inflammation: synovial fluid (SF) drained during therapeutic joint injection (JIA) and biopsies (mostly muscle, JDM). We discuss recent advances in the understanding of Treg biology in oligo-/ polyarticular JIA and JDM, and what we can learn about Treg-related disease mechanisms, treatments and biomarkers from other diseases
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