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. 2021 Dec 30;11(1):122. doi: 10.3390/cells11010122

Figure 2.

Figure 2

GILZ expression correlates with neutrophil activation state and functions. (A). GILZ ablation in GILZ-KO mice causes excessive neutrophil activation in response to inflammatory stimuli. Conversely, in WT mice, GILZ upregulation after activation inhibits the MAPK pathway and NOX2 (NADPH oxidase 2), reducing neutrophil activity. In a human cell line, GILZ upregulation caused apoptosis by upregulating JNK and downregulating Mcl-1. (B). The absence of GILZ in GILZ-KO mice with acute peritonitis prevents GC-dependent ANXA1 expression, whereas WT mice can express ANXA1, blocking neutrophil migration into inflamed tissues. By binding PU.1, GILZ promotes ANXA1 gene transcription. (C). GILZ treatment favors the development of N2 anti-inflammatory neutrophils in a model of AKI. (D). In vivo treatment with GC upregulates GILZ in circulating neutrophils, favoring its binding with STAT5 and downregulating TLR2 expression. The absence of GILZ maintains TLR2 levels, causing an excessive neutrophil response.