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Currently, there are two major theories for the pathogenesis of sepsis:hyperimmune and hypoimmune. Hyperimmune theory suggests that cytokine stormcauses the symptoms of sepsis. On the contrary, hypoimmune theory suggests thatimmunosuppression causes the manifestations of sepsis. By using microarraystudy, this study implies that hyperactivity of TH17-like innate immunity andfailure of adaptive immunity are noted in sepsis patients. I find out thatinnate immunity related genes are significantly up-regulated including CD14,TLR1,2,4,5,8, HSP70, CEBP proteins, AP1(JUNB, FOSL2), TGF-{\beta}, IL-6,TGF-{\alpha}, CSF2 receptor, TNFRSF1A, S100A binding proteins, CCR2, formylpeptide receptor2, amyloid proteins, pentraxin, defensins, CLEC5A, wholecomplement machinery, CPD, NCF, MMP, neutrophil elastase, caspases, IgG and IgAFc receptors(CD64, CD32), ALOX5, PTGS, LTB4R, LTA4H, and ICAM1. Majority ofadaptive immunity genes are down-regulated including MHC related genes, TCRgenes, granzymes/perforin, CD40, CD8, CD3, TCR signaling, BCR signaling, T & Bcell specific transcription factors, NK killer receptors, and TH17 helperspecific transcription factors(STAT3, RORA, REL). In addition, Treg relatedgenes are up-regulated including TGF{\beta}, IL-15, STAT5B, SMAD2/4, CD36, andthrombospondin. Thus, both hyperimmune and hypoimmune play important roles inthe pathophysiology of sepsis.

Sepsis is a syndrome with hyperactivity of TH17-like innate immunity and hypoactivity of adaptive immunity