“…Its function is uncertain, but in the exacerbation and continuation of the oral lichen planus, a cytokine complex network(such as TNF-α, IFN-γ, TGF-β, IL-1, 2, 4, 5, 6, 8, 10, 12, 17, 18, and IL-22) plays an significant role 5,14,18,[20][21][22] . Other researchers suggest that the cellmediated immune system starts with the expression of keratinocytes antigen; this step is accompanied by the movement of T cell lymphocytes directly activated by an antigen binding to the main histocompatibility complex (MHC)-1 on keratinocytes or activated CD4 + lymphocytes 13 .In exchange, the activated CD8 + T cells kill the basal keratinocytes by tumor necrosis factor (TNF)-alpha, Fas-FasLmediated or granzyme B-activated apoptosis 13 . Researchers conclude that oxidative stress influences molecules and pathways involved in the recruitment of lymphocytic infiltrates in OLP lesions and apoptosis induction, including ICAM-1, p53, TNF-alpha,NF-κB, Fas / FasL and granzyme B pathways 7,13 .Others assume that OLP 's inflammatory pathways activate T-cells to release reactive oxygen species ( ROS) alone or to enhance ROS production by activating keratinocytes, causing damage to neighboring cells 7 .…”