Regulatory (Treg) cells are key regulators of inflammation and important for immune tolerance and homeostasis. A major progress has been made in the identification and classification of Treg cells. Due to technological advances, we have gained deep insights in the epigenetic regulation of Treg cells. The use of fate reporter mice allowed addressing the functional consequences of loss of Foxp3 expression. Depending on the environment Treg cells gain effector functions upon loss of Foxp3 expression. However, the traditional view that Treg cells become necessarily pathogenic by gaining effector functions was challenged by recent findings and supports the notion of Treg cell lineage plasticity. Treg cell stability is also a major issue for Treg cell therapies. Clinical trials are designed to use polyclonal Treg cells as therapeutic tools. Here, we summarize the role of Treg cells in selected autoimmune diseases and recent advances in the field of Treg targeted therapies.

Treg cells in autoimmunity: from identification to Treg-based therapies

A cross talk between dysbiosis and gut-associated immune system governs the development of inflammatory arthropathies.

Spondyloarthritis (SpA), a type 3 immunity-mediated inflammatory arthritis, is a systemic rheumatic disease that primarily affects the joints, spine, gut, skin, and eyes. Macrophage migration inhib...

Macrophage migration inhibitory factor drives pathology in a mouse model of spondyloarthritis and is associated with human disease.

Ankylosing spondylitis is a complicated consequence of genetic predisposition and environmental factors. Enthesitis is believed to be the hallmark of ankylosing spondylitis, and the chronic inflammatory state of this disease is perpetuated by the disturbances of both the innate immune system and the acquired immune system. To clarify the alteration of immune system in patients with AS, we conducted a meta-analysis concerning the proportions of major lymphocyte subsets in the peripheral blood of AS patients. We systematically searched PubMed and China National Knowledge Infrastructure (CNKI) for articles related to this subject. A total of 95 articles involving 4,020 AS patients and 3,065 healthy controls were included in the analysis. This meta-analysis is performed on R platform using R package "meta", and Egger's tests were used to determine the presence of publication bias. Results showed that the percentages of T cells, NK cells and NKT cells were not significantly different between AS patients and healthy controls, but B cells were significantly increased. Among the subsets of T cells, the proportions of CD4+ T cells, Th17 cells, Tfh cells as well as Th1/Th2 ratio were significantly increased, while Tregs were significantly decreased. Subgroup analysis showed that the proportions of Th17 among both PBMCs, T cells and CD4+ T cells were significantly elevated, while Tregs were only significantly lower in PBMCs. Subgroup analysis also demonstrated that Tregs defined by "CD4+CD25+FoxP3+", "CD4+CD25+CD127low"or "CD4+CD25+CD127-"were significantly downregulated, indicating that the selection of markers could be critical. Further study is warranted in order to elucidate the complicated interactions between different lymphocyte subsets in AS patients. This study implied that the disequilibrium between Th17 and Tregs, as well as between Th1 and Th2 could contribute to the pathogenesis of ankylosing spondylitis, further cementing the understanding that ankylosing spondylitis is a consequence of disrupted balance of innate immune system and acquired immune system.

/pdf/imbalance-of-peripheral-lymphocyte-subsets-in-patients-with-zh7qoeo9bl.pdf

Imbalance of Peripheral Lymphocyte Subsets in Patients With Ankylosing Spondylitis: A Meta-Analysis.

Cluster of differentiation 226 (CD226) molecules play a crucial role in the activation of effector CD4+ T cells during the immune response process, but a cell-intrinsic function of CD226 in CD4+ T subsets is not clear. In this study, we showed that Cd226 -/- mice were resistant to myelin oligodendrocyte glycoprotein peptide 35-55 (MOG35-55)-induced experimental autoimmune encephalomyelitis (EAE) with highly expressed IL-10+CD4+ T cells and downregulated IL-17A+CD4+ T cells when compared with wild-type (WT) mice. Th17 cell infiltration into the central nervous system (CNS) was largely decreased in the absence of CD226 during EAE. CD226 deficiency facilitated the proliferation of regulatory T cells (Tregs), with increased numbers of Tregs observed in EAE mice, and supported the elevated induced regulatory T cell (iTregs) proliferation in vitro. The Akt and Erk signaling pathways were shown to be involved in Cd226 -/- Treg proliferation and function in vivo and in vitro. These findings collectively indicate that CD226 is a key molecule regulating the Treg-mediated suppression of autoimmune responses by inhibiting Treg proliferation. Thus, the results of this study identify additional mechanisms by which CD226 regulates Treg functions in EAE and supports the potential therapeutic effects of anti-CD226 molecules on autoimmune diseases.

CD226 Attenuates Treg Proliferation via Akt and Erk Signaling in an EAE Model.

Dysfunction of regulatory T cells in patients with ankylosing spondylitis is associated with a loss of Tim-3.

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Dysfunction of regulatory T cells in patients with ankylosing spondylitis is associated with a loss of Tim-3.