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In the BV2 cells (a mouse microglial cell line), Cu could trigger activation of the NF-B signaling pathway and increase the release of inflammatory factors such as nitric oxide (NO) and the cytokine tumor necrosis factor- (TNF-)

The etiology of UC is multifactorial, involving complex interactions among genetic predisposition, immune dysregulation, environmental factors, and gut microbiota alterations [10, 11]

Manufacturers may change their formulations, and this could alter compatibilities

This would suggest that the therapy with anti-classical IC (CTLA4 and PD1) is not appropriate as there is no possibility to relive the brake of the immune system

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