Products from human mast cell line cells enhance the production of interferon‐γ by CD8⁺ and CD4⁺ T cells

Abstract

SUMMARYIn patients with allergic asthma, T-cell cytokines are implicated in the regulation of the local inflammation in the airways. The ability of sensitized mast cells to release mediators and cytokines early upon allergen stimulation makes them important candidates for local immunoregulation. We have studied the effects of human mast cells on T cells with the use of the human mast cell line HMC-1. We showed that activated human mast cells or their soluble products induced and enhanced the interferon-c (IFN-c) production by T cells up to about 60-fold. The production of interleukin (IL)-4 was hardly affected and that of IL-5 was slightly enhanced. The enhancement of IFN-c production was induced both in polyclonal CD4 + and CD8 + T cells and in CD4 + and CD8 + T-cell clones. Further characterization of the factors involved demonstrated a molecular mass above 30 000. Our results implicate that by this mechanism mast cells may account for a negative feedback system locally down-regulating allergen-induced T helper 2 responses via IFN-c production by the T cells.

Quantification of mast cells in different stages of human periodontal disease

“…Still, there is a hypothesis that Th1 cells are associated with the stable lesion – gingivitis – while a Th2 response is linked to disease progression – periodontitis (Gemmell et al , 2002). The notion of a functional relationship between mast cells and T lymphocytes has been strengthened as activated mast cells reside in close apposition to T cells in some inflammatory processes (Bhattacharyya et al , 1998; Mekori and Metcalfe, 1999) and mast cells can secrete both Th2‐type (De Pater‐Huijsen et al , 1997; Hültner et al , 2000; Coulombe et al , 2002; De Pater‐Huijsen et al , 2002) and Th1‐type (Metcalfe et al , 1997; Tkaczyk et al , 2000) cytokines, influencing the differentiation of T cells (Robinson et al , 1993; Huels et al , 1995). Nevertheless, mast cells seem to be able to present antigens to T cells in vitro (Fox et al , 1994; Love et al , 1996; Malaviya et al , 1996; Villa et al , 2001).…”

Phenotypic changes in colonocytes following acute stress or activation of mast cells in mice: implications for delayed epithelial barrier dysfunction

“…17 Thus our results suggest a specific link between mast cell activation and IFN-c secretion by CD4+/ CD8+ T cells, as described in vitro. 33 Mast cells also release nerve growth factor which can play a role in the stress induced increase in CPP. 34 A 2-3 day delay has already been described in vitro for the effects of IFN-c on T84 cells to decrease levels of ZO-1 and to alter apical actin organisation, which leads to disorganisation of TJs and increased permeability.…”

Poor Outcomes of Chronic Active Epstein‐Barr Virus Infection and Hemophagocytic Lymphohistiocytosis in Non‐Japanese Adult Patients

“…Con-3 2.7 ϫ 10 sequently, CAEBV infection was considered to be the cause of his symptoms. Using fluorescence-activated cell sorting procedures, as described elsewhere [11], we demonstrated that the EBV load was confined to the natural killer cell compartment, and the patient was treated with high-dose dexamethasone, etoposide, and cyclosporine, followed by nonmyeloablative, allogeneic hematopoietic stem cell transplantation (HSCT) after induction with fludarabine and total body irradiation [12]. After an initial favorable response, EBV load rapidly increased (figure 1), and the patient developed severe electrolyte disturbances and thrombocytopenia.…”

“…A high EBV load of copies/mL was measured 6 15.0 ϫ 10 in the peripheral blood by quantitative PCR. Using cell sorting techniques [11], the EBV load was found to be located in the natural killer cell compartment. Bone marrow aspirate and biopsy results indicated hypercellular marrow with a reactive inflammatory response and hemophagocytosis.…”