Table 1.

Summary of studies on the pathophysiological significances of IL-17 in sepsis.

System	Year	Authors	Clinical observations or conclusions	References
Mice	2003	Tian et al.	CD4+ T cells mediated abscess formation in intra-abdominal sepsis by an IL-17-dependent mechanism	(35)
	2007	Shibata et al.	Resident Vδ1+ γδ T cells controlled early infiltration of neutrophils after Escherichia coli infection via IL-17 production	(36)
	2008	Flierl et al.	γδ T cell-derived IL-17 promoted high levels of proinflammatory mediators and bacteremia, increasing lethality	(37)
	2009	Freitas et al.	IL-17 enhanced the microbicidal activity of migrating neutrophils in sepsis induced by cecal ligation and puncture	(38)
	2010	Kasten et al.	IL-17 production by γδ T cells accelerated neutrophil recruitment in a sepsis model	(39)
	2012	Joshi et al.	Immunization with Staphylococcus aureus iron regulated surface determinant B conferred protection via Th17/IL-17 pathway	(40)
	2012	Ogiku et al.	IL-17A played a pivotal role in polymicrobial sepsis according to studies using IL-17 knockout mice	(41)
	2013	Bosmann et al.	Plasma concentrations of IL-17, IL-17F, and the IL-17AF heterodimer were obviously increased in mice after cecal ligation and puncture	(42)
	2014	Shimura et al.	IL-17, but not IL-17F or IL-25, was important to lipopolysaccharide-induced endotoxin shock; Myeloid cells and eosinohils, but not Th17 cells, was a source of IL-17 during endotoxin shock.	(43)
	2014	Jing et al.	Recombinant IL-17 rescued impaired host defense in cxcl1−/− mice; CXCL1 was important for IL-17 production via Th17 differentiation	(44)
	2014	Cauvi et al.	Elevated expression of IL-23/IL-17 pathway-related mediators correlated with exacerbation of pulmonary inflammation following polymicrobial sepsis	(45)
	2015	Costa et al.	Murine IL-17+Vγ4 T lymphocytes accumulated in the lungs and played a protective role in severe sepsis	(46)
	2015	Meng et al.	Activation of TLR2 by disseminated Gram-positive bacteria induced sustained upregulation of IL-17A and IL-6	(47)
	2016	Zhao et al.	Mice that completely lacked IL-17 failed to accumulate and activate neutrophils. Lung inflammation was attenuated in IL-17-deficient mice	(48)
	2016	Cen et al.	MFG-E8 downregulated IL-17 expression in sepsis by modulating STAT3 activation	(49)
	2016	Wynn et al.	IL-18 administration in sepsis increased IL-17A production by murine intestinal γδ T cells as well as Ly6G+ myeloid cells, and blocking IL-17A reduced IL-18-potentiated mortality in both neonatal sepsis and endotoxemia	(50)
	2016	Luo et al.	IL-17A knockout in mice protected against sepsis-associated acute kidney injury	(51)
	2017	Lv et al.	IL-33 attenuated sepsis by inhibiting IL-17 receptor signaling through upregulation of SOCS3	(52)
	2015	Szabo et al.	Rapid and rigorous IL-17A production by a distinct subpopulation of effector memory T lymphocytes constituted a novel mechanism of toxic shock syndrome immunopathology	(53)
Rats	2018	Han et al.	The levels of IL-17A in plasma, lung, and liver gradually increased with time in a sepsis neonatal rat model	(54)
Patients	2011	Makada et al.	IL-17A genetic variation was associated with altered susceptibility to Gram-positive infection and mortality in severe sepsis	(55)
	2011	Palumbo et al.	No significant associations were found between IL-6 and IL-17F genotypes and the related cytokine serum levels in burn patients with sepsis	(56)
	2015	Wu et al.	Treatment of anti-IL-17 enhanced IL-10 production but decreased IL-12 secretion in stimulated peripheral blood mononuclear cells of healthy controls and patients with severe sepsis	(57)
	2015	Paraschos et al.	Patients with multiple injuries showed defective TNF-α, IL-10, IL-17, and IFN-γ responses to a broad panel of bacterial stimuli	(58)
	2016	Maravistsa et al.	IL-17 was the only cytokine produced in high quantities by peripheral blood mononuclear cells and CD4+ lymphocytes in patients with septic shock and acute kidney injury	(59)
	2017	Preisser et al.	Increased IL-17 was noted in patients with sepsis-induced acute respiratory distress syndrome; IL-17 antibody administration might relieve acute lung injury symptoms by affecting RORγt levels and modulating the PI3K pathway.	(60)
	2017	Ali et al.	Elevated serum IL-17 increased the susceptibility for septic complications in polytrauma patients, and might be a useful biomarker of such risk	(61)