Anti‐inflammatory and immune‐modulatory impacts of berberine on activation of autoreactive T cells in autoimmune inflammation

Seyed‐Morteza Ehteshamfar(Mashhad University of Medical Sciences), Masoume Akhbari(Qazvin University of Medical Sciences), Jalil Tavakol Afshari(Mashhad University of Medical Sciences), Motahareh Seyedi(Yazd University), Banafsheh Nikfar(Iran University of Medical Sciences), Abbas Shapouri Moghaddam(Mashhad University of Medical Sciences), Erfan Ghanbarzadeh(Guilan University of Medical Sciences), Amir Abbas Momtazi‐Borojeni(Mashhad University of Medical Sciences)
Journal of Cellular and Molecular Medicine
November 1, 2020
Cited by 128Open Access
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Abstract

T regulatory (Treg) cells are crucial for the immune tolerance and have a critical role in the suppression of the excessive immune and inflammatory response promoted by these Th cells. In contrast, dendritic cells (DCs) and macrophages are immune cells that through their inflammatory functions promote autoreactive T-cell responses in autoimmune conditions. In recent years, there has been increasing attention to exploring effective immunomodulatory or anti-inflammatory agents from the herbal collection of traditional medicine. Berberine, an isoquinoline alkaloid, is one of the main active ingredients extracted from medicinal herbs and has been shown to exert various biological and pharmacological effects that are suggested to be mainly attributed to its anti-inflammatory and immunomodulatory properties. Several lines of experimental study have recently investigated the therapeutic potential of berberine for treating autoimmune conditions in animal models of human autoimmune diseases. Here, we aimed to seek mechanisms underlying immunomodulatory and anti-inflammatory effects of berberine on autoreactive inflammatory responses in autoimmune conditions. Reported data reveal that berberine can directly suppress functions and differentiation of pro-inflammatory Th1 and Th17 cells, and indirectly decrease Th cell-mediated inflammation through modulating or suppressing other cells assisting autoreactive inflammation, such as Tregs, DCs and macrophages.


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