Regulatory T cells control type I food allergy to Beta-lactoglobulin in mice.

Background: Regulatory T cells contribute to peripheral immune tolerance, yet their ability to control immediate-type hypersensitivity (ITH) reactions involved in IgE-mediated food allergy is still poorly documented.

Objectives: We investigated in mice whether CD4+CD25+ regulatory T cells could control ITH to β-lactoglobulin (BLG), a major allergen in cow's milk.

Methods: C3H/HeOuJ mice were sensitized by repeated oral gavage with BLG plus cholera toxin as adjuvant and orally challenged with BLG alone to elicit allergic symptoms.

Distinct and overlapping roles of interleukin-10 and CD25+ regulatory T cells in the inhibition of antitumor CD8 T-cell responses.

Lack of antitumor immunity is often related to impaired CD8 T-cell responses that could result from a poor priming capacity by tumor-infiltrating dendritic cells (TIDC) and/or further inhibition by regulatory T cells (T(reg)). Interleukin-10 (IL-10) has been implicated in the inhibition of TIDC as well as in the generation and functions of T(reg). Here, we address some of the respective and possibly overlapping roles of IL-10 and CD25+ T(reg) in CD8 antitumor immunity.

In vivo manipulation of dendritic cell migration and activation to elicit antitumour immunity.

Two approaches have been pursued to elicit antitumour immunity: (i) induce recruitment of immature dendritic cells or their precursors at a site of antigen delivery, and (ii) induce activation of tumour-infiltrating dendritic cells (DCs). The recruitment of selected DC subtype conditions the class of the immune response. Each immature DC population displays a unique spectrum of chemokine responsiveness.

Reversal of tumor-induced dendritic cell paralysis by CpG immunostimulatory oligonucleotide and anti-interleukin 10 receptor antibody.

Progressing tumors in man and mouse are often infiltrated by dendritic cells (DCs). Deficient antitumor immunity could be related to a lack of tumor-associated antigen (TAA) presentation by tumor-infiltrating DCs (TIDCs) or to a functional defect of TIDCs. Here we investigated the phenotype and function of TIDCs in transplantable and transgenic mouse tumor models.

Depletion of human NK and CD8 cells prior to in vitro H1N1 flu vaccine stimulation increases the number of gamma interferon-secreting cells compared to the initial undepleted population in an ELISPOT assay.

In order to study the respective roles of CD4, CD8, and CD56 (NK) cells in gamma interferon (IFN-gamma) production after in vitro stimulation with flu vaccine in a healthy adult human population, we depleted these cellular subtypes before stimulation with antigen (inactivated split vaccine, A/Texas H1N1, or A/Sydney H3N2). We observed that while CD4 cells were required for IFN-gamma secretion in both conditions in vitro, CD56 (NK) cells and, to a lesser extent, CD8 cells had a negative effect on such synthesis upon H1N1 stimulation, as judged by an increased number of spots compared to the initial undepleted population. This regulation of IFN-gamma secretion was associated with an increase in ICAM-1 expression, in particular on T and B cells.