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1.  Augmentation of regulatory B cell activity in experimental allergic encephalomyelitis by glatiramer acetate 
Journal of neuroimmunology  2010;232(0):136-144.
We recently showed that B cells reduce CNS inflammation in mice with experimental allergic encephalomyelitis (EAE). Here, we demonstrate that adoptively transferred CD5/CD19+ B cells protect against EAE severity. Furthermore, we show that glatiramer acetate (GA), a therapeutic for relapsing multiple sclerosis treatment, amplifies this effect. Transfer of GA-conditioned B cells leads to increased production of immunoregulatory cytokines and reduced CNS inflammation, as well as decreased expression of the chemokine receptor, CXCR5, and elevated BDNF expression in the CNS. Thus B cells can protect against EAE, and GA augments this effect in maintaining immune homeostasis and controlling EAE disease progression.
doi:10.1016/j.jneuroim.2010.10.031
PMCID: PMC3753076  PMID: 21111489
Glatiramer acetate; Inflammation; B cells; CD19; CD5
2.  Apoptosis in Toxoplasma gondii activated T cells: the role of IFNγ in enhanced alteration of Bcl-2 expression and mitochondrial membrane potential 
Microbial pathogenesis  2009;47(5):281-288.
In the present study we addressed the question whether Toxoplasma gondii could promote apoptosis in T lymphocytes in the acute stage of infection. Using in vivo activated T cells and then culturing them for a short time, we observed activation induced cell death in T. gondii infected mice. A higher level of activation induced cell death (AICD) was seen in susceptible C57BL/6 mice than in resistant CBA/J mice following infection with the same P strain of parasite. Apoptosis in T cells of susceptible mice was associated with altered induction of Bcl-2/Bax, loss of Mitochondrial Transmembrane Potential. Both CD4+ and CD8+ T cells were found to be susceptible to apoptosis; CD4+ T cells were sensitive to Fas mediated death whereas CD8+ T cells were insensitive to this signal. Caspase inhibitors had less effect on DNA fragmentation in CD4+ compared to CD8+ T cells. Exposure of CD4+ T cells to anti-IFNγ mAb resulted in an increase in the number of T cells that were positive for anti-apoptotic molecule Bcl-2 and DiOC6, a cationic dye that accumulates in intact mitochondria. These changes were less noticeable in CD8+ T cells following treatment with anti-IFNγ mAb. These findings provide further insight into the mechanisms of T cell apoptosis in T. gondii infection.
doi:10.1016/j.micpath.2009.09.004
PMCID: PMC2771447  PMID: 19748565
3.  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.
doi:10.1084/jem.20090246
PMCID: PMC2722185  PMID: 19596803

Results 1-3 (3)