43 research outputs found
MD2 ECONOMIC CONSEQUENCES OF PROVIDING RITUXIMAB AS ATREATMENT ALTERNATIVE FOR RHEUMATOID ARTHRITIS IN THE NETHERLANDS
Mediators produced by airway epithelial cells influence proliferation and differentiation of immature mast cells
CN3 PHARMACOECONOMIC (PE) ANALYSIS OF THE TREATMENT OF NON-SMALL CELL LUNG CANCER (NSCLC) IN THE NETHERLANDS DEMONSTRATES THAT ERLOTINIB DOMINATES DOCETAXEL AND IS COST-EFFECTIVE OVER BEST SUPPORTIVE CARE (BSC) WITHOUT NEED FOR PATIENT STRATIFICATION
PMS49 Cost-Effectiveness of Rituximab in the Treatment of RA Patients in the Netherlands
Mediators Produced by Airway Epithelial Cells Influence Proliferation and Differentiation of Immature Mast Cells
PCN41 ECONOMIC EVALUATION OF TRASTUZUMAB FOR THE ADJUVANT TREATMENT OF HER2 POSITIVE EARLY BREAST CANCER IN THE NETHERLANDS
PMS6 A Network Meta-analysis of Biologic Treatments in TNF-IR Rheumatoid Arthritis Patients
Products from mast cells influence T lymphocyte proliferation and cytokine production--relevant to allergic asthma?
In IgE allergic diseases both mast cells and T lymphocytes play an important role. Whereas mast cels have been implicated in immediate allergic responses, T lymphocytes mediate subsequent late phase responses and chronic inflammation. Here we review possible links between the early mast cell activation and the later T lymphocyte stimulation. Products from mast cells were found to exert effects on T lymphocytes. Human Mast Cell line-1 (HMC-1) mast cells modulated proliferation and cytokine production of a human CD8+ T-cell clone in vitro. Activated mast cells seemed to drive this CD8+ T-cell clone towards a more pronounced T (helper) 1 type of response, simultaneously decreasing T-cell numbers. It is hypothesized that this might be a negative feed back mechanism operating in allergic subjects, by which the Th2-driven IgE production and eosinophilia are counteracte