Persimmon leaf extract protects mice from atopic dermatitis by inhibiting T cell activation via regulation of the JNK pathway

2021 ◽  
Author(s):  
Hyun‐Su Lee ◽  
Eun‐Nam Kim ◽  
Ga‐Ram Kim ◽  
Gil‐Saeng Jeong
Keyword(s):  
Atopic Dermatitis ◽  
T Cell ◽  
T Cell Activation ◽  
Leaf Extract ◽  
Cell Activation ◽  
Jnk Pathway ◽  
Persimmon Leaf Extract ◽  
Persimmon Leaf

Suppression of T cell activation by hirsutenone, isolated from the bark of Alnus japonica, and its therapeutic advantages for atopic dermatitis

2009 ◽  
Vol 614 (1-3) ◽  
pp. 98-105 ◽  
Author(s):  
Seong Soo Joo ◽  
Sung Geun Kim ◽  
Sun Eun Choi ◽  
Yun-Bae Kim ◽  
Hee Yong Park ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Alnus Japonica

Atopic dermatitis: correlation of peripheral blood T cell activation, eosinophilia and serum factors with clinical severity

1993 ◽  
Vol 23 (2) ◽  
pp. 145-153 ◽  
Author(s):  
C. WALKER ◽  
M. K. KäGI ◽  
P. INGOLD ◽  
P. BRAUN ◽  
K. BLASER ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
T Cell ◽  
T Cell Activation ◽  
Peripheral Blood ◽  
Cell Activation ◽  
Clinical Severity ◽  
Serum Factors

Accelerated T-cell activation and differentiation of polar subsets characterizes early atopic dermatitis development

2016 ◽  
Vol 138 (5) ◽  
pp. 1473-1477.e5 ◽  
Author(s):  
Hitokazu Esaki ◽  
Tali Czarnowicki ◽  
Juana Gonzalez ◽  
Margeaux Oliva ◽  
Sreya Talasila ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation

Licoricidin Abrogates T Cell Activation by Modulating PTPN1 Activity and Attenuates Atopic Dermatitis In Vivo

2021 ◽  
Author(s):  
Hyun-Su Lee ◽  
Jooyoung Kim ◽  
Hyun Gyu Choi ◽  
Eun-Kyung Kim ◽  
Chang-Duk Jun
Keyword(s):  
Atopic Dermatitis ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation

scholarly journals Oral Administration of Liquiritigenin Confers Protection from Atopic Dermatitis through the Inhibition of T Cell Activation

Biomolecules ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 786
Author(s):  
Hyun-Su Lee ◽  
Eun-Nam Kim ◽  
Gil-Saeng Jeong
Keyword(s):  
T Cells ◽  
Atopic Dermatitis ◽  
T Cell ◽  
Oral Administration ◽  
T Cell Activation ◽  
Cell Activation ◽  
Therapeutic Potential ◽  
Activated T Cells

While liquiritigenin, isolated from Spatholobus suberectus Dunn, is known to possess anti-inflammatory activities, it still remains to be known whether liquiritigenin has a suppressive effect on T cell activation and T cell-mediated disease. Here, we used Jurkat T cells to explore an underlying mechanism of pre-treatment with liquiritigenin in activated T cell in vitro and used atopic dermatitis (AD) in vivo to confirm it. We found liquiritigenin blocks IL-2 and CD69 expression from activated T cells by PMA/A23187 or anti-CD3/CD28 antibodies. The expressions of surface molecules, including CD40L and CD25, were also reduced in activated T cells pre-treated with liquiritigenin. Western blot analysis indicated repressive effects by liquiritigenin are involved in NFκB and MAPK pathways. To assess the effects of liquiritigenin in vivo, an AD model was applied as T cell-mediated disease. Oral administration of liquiritigenin attenuates AD manifestations, including ear thickness, IgE level, and thicknesses of dermis and epidermis. Systemic protections by liquiritigenin were observed to be declined in size and weight of draining lymph nodes (dLNs) and expressions of effector cytokines from CD4+ T cells in dLNs. These results suggest liquiritigenin has an anti-atopic effect via control of T cell activation and exhibits therapeutic potential for T cell-mediated disorders.

scholarly journals Regulation of c-Jun NH2-terminal Kinase ( Jnk) Gene Expression during T Cell Activation

2000 ◽  
Vol 191 (1) ◽  
pp. 139-146 ◽  
Author(s):  
Linda Weiss ◽  
Alan J. Whitmarsh ◽  
Derek D. Yang ◽  
Mercedes Rincón ◽  
Roger J. Davis ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cell ◽  
T Cell Activation ◽  
Map Kinases ◽  
Cell Activation ◽  
Cell Receptor ◽  
Jnk Pathway ◽  
Gene And Protein Expression

The c-Jun NH2-terminal kinases (JNKs) are a group of mitogen-activated protein (MAP) kinases that participate in signal transduction events mediating specific cellular functions. Activation of JNK is regulated by phosphorylation in response to cellular stress and inflammatory cytokines. Here, we demonstrate that JNK is regulated by a second, novel mechanism. Induction of Jnk gene expression is required in specific tissues before activation of this signaling pathway. The in vivo and in vitro ligation of the T cell receptor (TCR) leads to induction of JNK gene and protein expression. TCR signals are sufficient to induce JNK expression, whereas JNK phosphorylation also requires CD28-mediated costimulatory signals. Therefore, both expression and activation contribute to the regulation of the JNK pathway to ensure proper control during the course of an immune response.

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