Background: IL-17 and Foxp3 double-expressing (DE) CD4 + T lymphocytes are novel crossover immune cell population, but the presence and role of these cells in human intestinal inflammation is unclear. The aim of this study was to investigate the circulating IL-17 and Foxp3 DE CD4 + T lymphocytes in patients with inflammatory bowel disease (IBD). Methods: The entire cohort consisted of 79 subjects: 31 patients with Crohn’s disease, 28 patients with ulcerative colitis, and 20 healthy control subjects (HC). IBD patients with evidence of active disease at endoscopy were entered into the study. Peripheral blood mononuclear cells were used for ex vivo and in vitro studies to assess the characteristics and generation of these novel cells and the function of circulating Foxp3 + CD4 + regulatory T lymphocytes (Treg) in patients with IBD compared with HC. Results: Patients with IBD had significantly higher prevalence of IL-17 and Foxp3 DE CD4 + T lymphocytes compared with age- and gender-matched HC. These cells expressed RORgt. The ability of Treg cells to suppress autologous T-cell proliferation was reduced by approximately 60% in patients with IBD compared with HC. Increased generation of these DE cells was demonstrated by the modulation of cytokine environment of CD4 + lymphocytes in vitro in patients with Crohn’s disease. Conclusions: Prevalence of circulating IL-17 and Foxp3 DE CD4 + T cells is increased in patients with IBD. Coexpression of RORg ta nd Foxp3 in these cells implies conversion from Treg cells to Th17 cells. This is associated with a decreased suppressive function of Foxp3 + CD4 + T lymphocytes in patients with IBD. (Inflamm Bowel Dis 2013;19:2522–2534)

/pdf/increased-prevalence-of-circulating-novel-il-17-secreting-ivzrtv0bpj.pdf

Increased prevalence of circulating novel IL-17 secreting Foxp3 expressing CD4+ T cells and defective suppressive function of circulating Foxp3+ regulatory cells support plasticity between Th17 and regulatory T cells in inflammatory bowel disease patients

In vitro differentiated CD8+ T cells have been the primary focus of immunotherapy of cancer with little focus on CD4+ T cells. Immunotherapy involving in vitro differentiated T cells given after lymphodepleting regimens significantly augments antitumor immunity in animals and human patients with cancer. However, the mechanisms by which lymphopenia augments adoptive cell therapy and the means of properly differentiating T cells in vitro are still emerging. We demonstrate that naive tumor/self-specific CD4+ T cells naturally differentiated into T helper type 1 cytotoxic T cells in vivo and caused the regression of established tumors and depigmentation in lymphopenic hosts. Therapy was independent of vaccination, exogenous cytokine support, CD8+, B, natural killer (NK), and NKT cells. Proper activation of CD4+ T cells in vivo was important for tumor clearance, as naive tumor-specific CD4+ T cells could not completely treat tumor in lymphopenic common gamma chain (γc)–deficient hosts. γc signaling in the tumor-bearing host was important for survival and proper differentiation of adoptively transferred tumor-specific CD4+ T cells. Thus, these data provide a platform for designing immunotherapies that incorporate tumor/self-reactive CD4+ T cells.

/pdf/naive-tumor-specific-cd4-t-cells-differentiated-in-vivo-3vloq6qtex.pdf

Naive tumor-specific CD4+ T cells differentiated in vivo eradicate established melanoma

Editorial overview: lymphocyte development.

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Editorial overview: lymphocyte development.

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Increased prevalence of circulating novel IL-17 secreting Foxp3 expressing CD4+ T cells and defective suppressive function of circulating Foxp3+ regulatory cells support plasticity between Th17 and regulatory T cells in inflammatory bowel disease patients

Naive tumor-specific CD4+ T cells differentiated in vivo eradicate established melanoma