  Currently, there are two major theories for the pathogenesis of sepsis:
hyperimmune and hypoimmune. Hyperimmune theory suggests that cytokine storm
causes the symptoms of sepsis. On the contrary, hypoimmune theory suggests that
immunosuppression causes the manifestations of sepsis. By using microarray
study, this study implies that hyperactivity of TH17-like innate immunity and
failure of adaptive immunity are noted in sepsis patients. I find out that
innate 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, formyl
peptide receptor2, amyloid proteins, pentraxin, defensins, CLEC5A, whole
complement machinery, CPD, NCF, MMP, neutrophil elastase, caspases, IgG and IgA
Fc receptors(CD64, CD32), ALOX5, PTGS, LTB4R, LTA4H, and ICAM1. Majority of
adaptive immunity genes are down-regulated including MHC related genes, TCR
genes, granzymes/perforin, CD40, CD8, CD3, TCR signaling, BCR signaling, T & B
cell specific transcription factors, NK killer receptors, and TH17 helper
specific transcription factors(STAT3, RORA, REL). In addition, Treg related
genes are up-regulated including TGF{\beta}, IL-15, STAT5B, SMAD2/4, CD36, and
thrombospondin. Thus, both hyperimmune and hypoimmune play important roles in
the pathophysiology of sepsis.
