title: IL-36 signaling amplifies Th1 responses by enhancing proliferation and Th1 polarization of naive CD4+ T cells.
abstract: The interleukin-1 (IL-1) superfamily of cytokines comprises a set of pivotal mediators of inflammation. Among them, the action of IL-36 cytokines in immune responses has remained elusive. In a recent study, we demonstrated a direct effect of IL-36 on immune cells. Here we show that, among T cells, the IL-36 receptor is predominantly expressed on naive CD4(+) T cells and that IL-36 cytokines act directly on naive T cells by enhancing both cell proliferation and IL-2 secretion. IL-36β acts in synergy with IL-12 to promote Th1 polarization and IL-36 signaling is also involved in mediating Th1 immune responses to Bacillus Calmette-Guerin infection in vivo. Our findings point toward a critical function of IL-36 in the priming of Th1 cell responses in vitro, and in adaptive immunity in a model of mycobacterial infection in vivo.
authors.affiliation: Division of Rheumatology, Department of Internal Medicine, University of Geneva School of Medicine, Switzerland.
authors.forename: Solenne
authors.initials: S
authors.lastname: Vigne
authors.forename: Gaby
authors.initials: G
authors.lastname: Palmer
authors.forename: Praxedis
authors.initials: P
authors.lastname: Martin
authors.forename: Céline
authors.initials: C
authors.lastname: Lamacchia
authors.forename: Deborah
authors.initials: D
authors.lastname: Strebel
authors.forename: Emiliana
authors.initials: E
authors.lastname: Rodriguez
authors.forename: Maria L
authors.initials: ML
authors.lastname: Olleros
authors.forename: Dominique
authors.initials: D
authors.lastname: Vesin
authors.forename: Irene
authors.initials: I
authors.lastname: Garcia
authors.forename: Francesca
authors.initials: F
authors.lastname: Ronchi
authors.forename: Federica
authors.initials: F
authors.lastname: Sallusto
authors.forename: John E
authors.initials: JE
authors.lastname: Sims
authors.forename: Cem
authors.initials: C
authors.lastname: Gabay
mesh_terms: D056704:Adaptive Immunity; D000818:Animals; D002454:Cell Differentiation; D049109:Cell Proliferation; D007375:Interleukin-1 / Q000276:immunology / Q000494:pharmacology; D018664:Interleukin-12 / Q000276:immunology / Q000494:pharmacology; D007376:Interleukin-2 / Q000096:biosynthesis / Q000276:immunology; D008213:Lymphocyte Activation; D051379:Mice; D018345:Mice, Knockout; D009163:Mycobacterium bovis / Q000276:immunology*; D061251:Primary Cell Culture; D017472:Receptors, Interleukin-1 / Q000172:deficiency / Q000235:genetics / Q000276:immunology*; D015398:Signal Transduction / Q000235:genetics / Q000276:immunology*; D018417:Th1 Cells / Q000166:cytology / Q000276:immunology* / Q000382:microbiology; D014376:Tuberculosis / Q000235:genetics / Q000276:immunology / Q000378:metabolism* / Q000662:veterinary*
chemical_list: D007375:Interleukin-1; D018664:Interleukin-12; D007376:Interleukin-2; D017472:Receptors, Interleukin-1; C502352:IL-1F8 protein, mouse; C543716:interleukin 1F6, mouse; C569500:Il1rl2 protein, mouse