20 research outputs found

    Dendritic cells from Peyer's patch and spleen induce different T helper cell responses

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    The role of antigen-presenting cells (APC) in regulating the balance of T helper type 1 (Th1) and T helper 2 (Th2) responses and cytokine production is unclear. Dendritic cells (DC), the most potent APC for naive T cell activation, were found to regulate Th1 and Th2 cytokine profiles in a manner dependent on their tissue of origin. Using whole tissues or purified cell mixtures, spleen (systemic) DC were found to induce mainly Th1 cytokines, and Peyer's patch (mucosal) DC were found to induce predominantly Th2 cytokines. Spleen DC induced high levels of interferon-γ (IFN-γ) or interleukin-2 (IL- 2) or both, and Peyer's patch DC induced IL-4 or IL-6 or both in spleen and Peyer's patch T cells, allogeneic mixed leukocyte reactions, or antigen- specific Th0 clones. These data suggest that the tissue of origin of DC has a significant impact on subsequent T cell development.</p

    Protein-kinase-specific inhibitors block Langerhans’ cell migration by inhibiting interleukin-1α release

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    Previous studies have shown that depletion of Langerhans’ cells (LC) from murine epidermis by the superantigen, staphylococcal enterotoxin A (SEA) involves interleukin-1α (IL-1α) and is inhibitable by agents that block G-protein-associated kinases. The purpose of this study was to determine whether specific kinase inhibitors block LC depletion by inhibiting IL-1α release and to ascertain whether LC depletion by SEA involves cell migration. These goals were addressed by measuring the IL-1α release within whole or LC-depleted epidermal cell suspensions in the presence of SEA and/or H-7 (an inhibitor of protein kinase C) or H-8 (an inhibitor of G-protein-associated kinases) and by examining the migration of cells with LC markers in SEA-treated skin sections. The results suggest that LC depletion by SEA involves migration and that this migration is blocked by protein kinase inhibitors, at least in part, through inhibition of SEA-induced IL-1α release by epidermal cells
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