TNFSF14 coordinately enhances CXCL10 and CXCL11 productions from IFN-gamma-stimulated human gingival fibroblasts

Molecular Immunology
Yoshitaka HosokawaTakashi Matsuo

Abstract

TNFSF14 is involved in the pathogenesis of some inflammatory diseases such as arthritis. CXCL10 and CXCL11 recruit Th1 cells, and the productions of these chemokines are related to the exacerbation of some inflammatory diseases including arthritis and periodontal disease. We examined in vitro effects of TNFSF14 on IFN-gamma-induced CXCL10 and CXCL11 production in human gingival fibroblasts (HGFs). HGFs constitutively expressed TNFSF14 receptors, LTbetaR and HVEM. TNFSF14 enhanced IFN-gamma-induced secretion of CXCL10 and CXCL11 from HGFs. IFN-gamma treatment increased HVEM expression on HGFs. TNFSF14 in combination with IFN-gamma resulted in increased activation of p38 MAPK, ERK and IkappaB-alpha compared with TNFSF14 or IFN-gamma alone. Moreover, inhibitors of p38 MAPK, ERK and NF-kappaB abolished the CXCL10 and CXCL11 productions from TNFSF14 with IFN-gamma-stimulated HGFs. These effects of TNFSF14 may promote the infiltration of Th1 cells into lesions with inflammatory diseases. TNFSF14 might act as a proinflammatory cytokine in some inflammatory diseases thus is a candidate therapeutic target.

References

Apr 1, 1996·Journal of Periodontal Research·Y ShimabukuroH Okada
May 7, 2002·Journal of Periodontology·Farzaneh DaghighJoseph H Bee
May 28, 2003·Biochemical and Biophysical Research Communications·Pao-Li WangJunzo Tanaka
Nov 18, 2004·Immunological Reviews·Kirsten SchneiderCarl F Ware
Jan 4, 2007·The American Journal of Pathology·Philip StashenkoAntonio Campos-Neto

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Citations

Nov 24, 2011·Clinical & Developmental Immunology·Boel De PaepeJan L De Bleecker
Aug 29, 2018·Journal of Periodontal Research·Rebecca PeyyalaJeffrey L Ebersole
Nov 9, 2018·Molecular Oral Microbiology·Jeffrey L EbersoleOctavio A Gonzalez
Mar 29, 2011·Clinical and Experimental Immunology·Z LiuP-C Yang

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