IL-36 signaling amplifies Th1 responses by enhancing proliferation and Th1 polarization of naive CD4+ T cells.
- Vigne S Division of Rheumatology, Department of Internal Medicine, University of Geneva School of Medicine, Switzerland.
- Palmer G
- Martin P
- Lamacchia C
- Strebel D
- Rodriguez E
- Olleros ML
- Vesin D
- Garcia I
- Ronchi F
- Sallusto F
- Sims JE
- Gabay C
- 2012-09-13
Published in:
- Blood. - 2012
Adaptive Immunity
Animals
Cell Differentiation
Cell Proliferation
Interleukin-1
Interleukin-12
Interleukin-2
Lymphocyte Activation
Mice
Mice, Knockout
Mycobacterium bovis
Primary Cell Culture
Receptors, Interleukin-1
Signal Transduction
Th1 Cells
Tuberculosis
English
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.
- Language
-
- English
- Open access status
- bronze
- Identifiers
-
- DOI 10.1182/blood-2012-06-439026
- PMID 22968459
- Persistent URL
- https://sonar.ch/global/documents/170904
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