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1.  IL-9 as a mediator of Th17-driven inflammatory disease 
The Journal of Experimental Medicine  2009;206(8):1653-1660.
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.
PMCID: PMC2722185  PMID: 19596803
2.  PD-1 ligands expressed on myeloid-derived APC in the CNS regulate T cell responses in EAE 
European journal of immunology  2008;38(10):2706-2717.
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.
PMCID: PMC2727707  PMID: 18825752
antigen presenting cells; autoimmunity; costimulatory molecules; dendritic cells; inhibitory receptors

Results 1-2 (2)