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European journal of immunology (1)
The Journal of Experimental Medicine (1)
Schreiner, Bettina (2)
Bailey, Samantha L. (1)
Becher, Burkhard (1)
Begum-Haque, Sakhina (1)
Chen, Lieping (1)
Coyle, Anthony J. (1)
Kasper, Lloyd H. (1)
Miller, Stephen D. (1)
Noelle, Randolph J. (1)
Nowak, Elizabeth C. (1)
Shin, Tahiro (1)
Turner, Henrietta (1)
Weaver, Casey T. (1)
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IL-9 as a mediator of Th17-driven inflammatory disease
Nowak, Elizabeth C.
Weaver, Casey T.
Coyle, Anthony J.
Kasper, Lloyd H.
Noelle, Randolph J.
The Journal of Experimental Medicine
We report that like other T cells cultured in the presence of transforming growth factor (TGF) β, Th17 cells also produce interleukin (IL) 9. Th17 cells generated in vitro with IL-6 and TGF-β as well as purified ex vivo Th17 cells both produced IL-9. To determine if IL-9 has functional consequences in Th17-mediated inflammatory disease, we evaluated the role of IL-9 in the development and progression of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. The data show that IL-9 neutralization and IL-9 receptor deficiency attenuates disease, and this correlates with decreases in Th17 cells and IL-6–producing macrophages in the central nervous system, as well as mast cell numbers in the regional lymph nodes. Collectively, these data implicate IL-9 as a Th17-derived cytokine that can contribute to inflammatory disease.
PD-1 ligands expressed on myeloid-derived APC in the CNS regulate T cell responses in EAE
Bailey, Samantha L.
Miller, Stephen D.
European journal of immunology
Disease progression in EAE is regulated by PD-1 and its ligands, B7-H1 (PD-L1) and B7-DC (PD-L2). B7-H1 and B7-DC, have negative regulatory affects upon binding PD-1 on activated T cells and B7-H1 deficiency increases severity of both diabetes and EAE. However the role of PD-L expression on different APC in the CNS in regulating local T cell function during relapsing EAE (R-EAE) has not been examined. Our data show that the majority of CNS CD4+ T cells isolated during acute EAE are PD-1+, and T cells specific for relapse-associated epitopes express PD-1 upon antigen-stimulation in the CNS. B7-H1 and B7-DC are differentially expressed on discrete APC populations in the inflamed CNS. B7-H1 and PD-1 have mainly inhibitory functions on CNS T cells. B7-H1 negatively regulates the stimulation of activated PD-1+ TH cells, in co-cultures with microglia and different CNS-infiltrating APC presenting endogenously processed peptides. The preponderance of IFN-γ+ versus IL-17+ T cells in the CNS of B7-H1−/− mice suggests that B7-H1 more selectively suppresses TH-1 than TH-17 responses in vivo. In contrast, blockade of B7-DC has less pronounced regulatory effects. Overall, the results demonstrate that B7-H1 expressed by CNS myeloid APC negatively regulates T cell activation during acute R-EAE.
antigen presenting cells; autoimmunity; costimulatory molecules; dendritic cells; inhibitory receptors
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