Immunosuppression after sepsis has been described as compensatory anti-inflammatory response syndrome27, and is regulated by co-stimulatory molecules such as CD80/B7-1, which are produced by activation of the TLR signaling pathway, and the naive T cells transformed into regulatory T cells induced by cytokines, and this results in a reduced expression of antigen presentation-related transcription factors (e.g., IRF4, MUM1) [45,46,47]. This evidence concerns the gene IRF4 and Sepsis.