The immune system is indispensable for defense against invading pathogens, but its aberrant activation may lead to autoimmune diseases. Regulatory T cells play a crucial role in preventing excess immune activation; mice without enough Treg function develop autoimmune disorders and are susceptible to immune diseases.
“Treg cells have been attracting much attention due to their unique suppressive function, but how Treg cells are generated in our bodies is not fully understood. In a mouse model for human ulcerative colitis, mice lacking JunB developed more severe symptoms due to reduction of Treg cell number. JunB-deficient T cells exhibited an impairment of IL-2 production and IL-2 signaling. In addition, injection of a high dose of IL-2 into JunB-deficient mice mitigated colitis by expansion of Treg cells,” explained the lead author of the paper, Takaharu Katagiri, M.D., who is a graduate student at Toho University working to become a physician-scientist.
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