IL-21 promotes allergic airway inflammation by driving apoptosis of FoxP3+ regulatory T cells

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Phosphatase wild-type p53-induced phosphatase 1 controls the development of TH9 cells and allergic airway inflammation

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Activated plasmacytoid dendritic cells regulate type 2 innate lymphoid cell–mediated airway hyperreactivity

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Inhibitory checkpoint receptors control CD8+ resident memory T cells to prevent skin allergy

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Critical role of plasmacytoid dendritic cells in induction of oral tolerance

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New insights for regulatory T cell in lupus nephritis

Lupus nephritis (LN) is a complicated autoimmune disease marked by out-of-balance of immunological reactivity and immune tolerance. With the advance of immunotherapy in human disease, regulatory T (Treg) cells serve a crucial function in immune tolerance regulation and are characterized with suppression function as one of the most important research hotspots for autoimmunity diseases. In recent years, Treg cells have shown the robust potential for treatment to autoimmunity diseases like type I diabetic mellitus and rheumatoid arthritis. However, Treg cell therapy is poorly understood for LN patients. This review aims to summarize new insights for Treg-targeting techniques in LN patients. The current data regarding the biology features of Treg cells in LN patients is discussed. The propotion of Treg cells in LN patients have contradictory results regarding the use of different molecular markers. Forkhead box protein 3 (FOXP3) are hallmarks for control function of Treg cells. Treg cells can directly or indirectly target T cells and B cells by playing supressive role. The molecular targets for Treg cells in LN patients includes gene variants, miRNAs, and inflammatory related factors. Based on the current knowledge of Treg cell biology, several therapeutic strategies could be used to treat LN: cell transplantation, low dose IL-2 treatment, drugs target the balance of Treg and type 17 T helper (Th17) cells, and Chinese medicine.