Qiong Huang

Foxp3+ regulatory T cells and related cytokines differentially expressed in plaque vs. guttate psoriasis vulgaris

Background  Differences in the number of Foxp3+ regulatory T cells (Tregs) in lesional skin and peripheral blood and their functioning in plaque vs. guttate psoriasis have not been reported.

Dysregulation of miRNA146a versus IRAK1 induces IL-17 persistence in the psoriatic skin lesions

Psoriasis is a common chronic inflammatory skin disorder with dysregulation of miRNAs. The expression pattern of miR-146a and target gene IRAK1 in lesions and PBMCs of plaque psoriasis remains unclear. In our study, we found the expression of miR-146a was up-regulated both in lesions and PBMCs of psoriatic patients, and positively correlated with IL-17 expression, whereas the target gene IRAK1 expression was expressed differentially in lesions and peripheral blood. Inability of miR-146a inhibiting target gene IRAK1 may contribute to the persistent inflammation in lesions of psoriasis.

Evaluation of 308‐nm monochromatic excimer light in the treatment of psoriasis vulgaris and palmoplantar psoriasis

Background: The purpose of this study is to evaluate the efficacy and safety of 308‐nm monochromatic excimer light (MEL) in the treatment of psoriasis vulgaris and palmoplantar psoriasis.

Target tissue ectoenzyme CD39/CD73-expressing Foxp3+ regulatory T cells in patients with psoriasis.

Psoriasis is a chronic, relapsing, inflammatory skin disease, in which regulatory T cells (Tregs) play an important role. Recently, human Treg ectoenzymes (CD39/CD73) have been reported to mediate the suppressive activity of Tregs.

IgE and FcεRI are highly expressed on innate cells in psoriasis.

Although elevated serum IgE levels have been reported in psoriasis, the role of IgE in psoriasis still needs to be clarified.

Methotrexate restores the function of peripheral blood regulatory T cells in psoriasis vulgaris via the CD73/AMPK/mTOR pathway

Methotrexate (MTX) is used to treat psoriasis, a chronic inflammatory skin disease.

Phenotypical analysis of ectoenzymes CD39/CD73 and adenosine receptor 2A in CD4+CD25highFoxp3+ regulatory T‐cells in psoriasis

CD39 and CD73 are two novel cell surface markers of CD25highFoxp3+ regulatory T‐cells (Tregs). Concordant expression of these two ectoenzymes not only discriminate Tregs from other cell populations, but also generates pericellular adenosine, which has been reported to suppress proliferation of activated T effector (Teff) cells. Because it is currently unclear whether human ectoenzymes (CD39/CD73) are involved in the impaired suppressive activity of Tregs in psoriasis, we examined the frequencies and phenotypes of CD39/CD73‐expressing Tregs and related receptor adenosine receptor 2A (A2AR) in peripheral blood of patients with different types of psoriasis.

The distinct role and regulatory mechanism of IL-17 and IFN-γ in the initiation and development of plaque vs guttate psoriasis

BACKGROUND Few studies have explored the differences of immunopathogenesis in plaque vs guttate psoriasis, especially on the inhibitory role of regulatory T cells (Tregs) on IL-17/ IFN-γ production and the impact of CD4+T cells on keratinocytes. OBJECTIVE To investigate the percentage and inhibitory function of CD4+CD25highTreg and differential expressions of IL-17/ IFN-γ in plaque vs guttate psoriasis, and the effects of CD4+T cells on the proliferation of keratinocytes. METHODS Peripheral blood mononuclear cells (PBMCs) were prepared from patients with the plaque and guttate psoriasis. The percentage of CD4+CD25high Tregs, IL-17/IFN-γ- producing CD4+ or CD8+T cells, and apoptosis and cell cycle of Hacat cells were determined by flow cytometry. The level of IFN-γ in supernatants was analyzed by ELISA. RESULTS The percentage of CD4+CD25highTregs in plaque psoriasis was significantly increased, and they can inhibit IFN-γ production from CD4+CD25- effector T cells. The percentage of CD8+IFN-γ+cells was also significantly increased in plaque psoriasis, and these cells positively correlated with disease severity. The percentage of CD4+CD25highTregs was decreased and CD4+IFN-γ+/IFN-γ+IL-17+ cells were predominantly increased in guttate psoriasis. CD4+T cells from guttate psoriasis induce apoptosis of keratinocytes while they promote the proliferation of keratinocytes in plaque psoriasis by decreasing late apoptosis and increasing the percentage of G1 phase. CONCLUSION There was considerable discrepancy of the phenotype and function of T cells between plaque vs guttate psoriasis. IFN-γ and IL-17 from CD4+T cells play a crucial role in guttate psoriasis, however, IFN-γ and IL-17 from CD8+T cells are more important in the immunopathogenesis of plaque psoriasis.

Methotrexate activated Tregs via the CD73/AMPK/mTOR pathway

Psoriasis is a common skin disease that affects about 2% to 3% of people. The cause is unknown and believed to involve the genes and immune system, and the treatments we use now can control psoriasis but do not cure it. This study, from China, aimed to find out the effect and mechanism (way of working) of a drug called methotrexate on cells called regulatory T cells, which have the power to fight back and calm down the skin, as well as its relationship with the pathway of a chemical in the body called adenosine, which is a target in psoriasis therapy. Regulatory T cells (and effector T cells, which can trigger psoriasis) were isolated from the blood of healthy people and patients with psoriasis. Various laboratory tests were used to examine the effect of methotrexate on the adenosine pathway. The authors found that psoriasis patients have regulatory T cells with decreased function, meaning they do not work so well, and reduced CD73 level, which was the starting section of adenosine pathway. Furthermore, methotrexate could restore the immunosuppressive function of regulatory T cells by affecting part of the adenosine pathway, including increasing CD73 expression and regulating its related signal pathway. In conclusion, the study deepens doctors’ and patients’ understanding of methotrexate in the treatment of psoriasis, and contributes to our understanding of psoriasis.