“…Most probably, microorganisms could trigger TLR3/ TLR4, which expression is increased in KCs of PF patients leading to NF-kB activation [37]. The activation of TLR pathways leads to proinflammatory cytokine secretion, which could maintain the chronic activation of the CD4+ T-cell in PF [38,39]. Thus, after stimulation by bacterial products, TLRs mediate a variety of signals not only for inducing pro-inflammatory cytokines, such as TNF-α, IL-6, INF-γ, and IL-12, but also for up-regulated co-stimulatory molecules, such as CD80 and CD86 to activate immune responses [40].…”