Monocyte Chemotactic Protein 1 Regulates Oral Tolerance Induction by Inhibition of T Helper Cell 1–related Cytokines

Oral tolerance for delayed type hypersensitivity contribution of local and peripheral mechanisms

Oral tolerance is a physiological immune mechanism, which controls the outcome of deleterious hypersensitivity reactions to environmental antigens absorbed through the gastrointestinal tract, and maintains homeostasis. Using a mouse model of oral tolerance of delayed type hypersensitivity to contact allergens, i.e. haptens, we have examined the mechanisms involved in the induction of oral toler...

Polarized subsets of human T-helper cells induce distinct patterns of chemokine production by normal and systemic sclerosis dermal fibroblasts

The role of fibroblasts in inflammatory processes and their cross-talk with T cells is increasingly being recognized. Our aim was to explore the capacity of dermal fibroblasts to produce inflammatory chemokines potentially involved in fibrosis occurring in response to contact with polarized human T cells. Our findings indicate that the program of chemokine production by fibroblasts is different...

Monocyte Chemoattractant Protein-1- and Induction of Low Dose Oral Tolerance in

Expression of multiple chemokine genes by a human mast cell leukemia.

The chemokines are a large group of cytokines that are recognized to be important mediators of inflammation. In this study we show that the human mast cell leukemia line HMC-1 is a source of multiple chemokines, including I-309, monocyte chemoattractant protein 1, macrophage inflammatory protein-1 alpha, macrophage inflammatory protein-1 beta, RANTES, and interleukin-8. I-309 and MCP-1 transcri...

T-bet is induced by interferon-γ to mediate chemokine secretion and migration in human airway smooth muscle cells.

An inappropriate balance between T-helper (Th)1 and Th2 cytokine production underlies inflammatory changes that result in airway disease. Expression of the T-box transcription factor T-bet regulates differentiation of Th cells and production of Th1 cytokines, particularly IFNγ. T-bet-deficient mice develop airway hyperreactivity, undergo airway remodeling, and exhibit defects in IFNγ production...