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L S van Rijt

Publications and source records attributed to L S van Rijt.

2 recordsLinked to original sources

Dendritic cells in asthma: a function beyond sensitization.

Allergic asthma is one of the most common chronic diseases in western society, characterized by variable airway obstruction, mucus hypersecretion and infiltration of the airway wall with T-helper type 2 (Th2) cells, eosinophils and mast cells. If we are to devise new causal therapies for this disease, it is important to elucidate how Th2 cells are activated and respond to intrinsically harmless allergens. Dendritic cells (DCs) are the most important antigen-presenting cells in the lung and are mainly recognized for their exceptional potential to generate a primary immune response and sensitization to aeroallergens. Much less attention has been paid to the role of DCs in established inflammation. Based on functional studies in a murine model for asthma, in this review article, we propose that DCs are essential for generating allergen-specific effector Th2 responses in ongoing inflammation in sensitized mice. A better understanding of the role of DCs in the maintenance of the inflammatory response to allergens in asthma should lead to new therapeutic approaches intervening at the top of the inflammatory cascade.

Allergens↗

Role of dendritic cells and Th2 lymphocytes in asthma: lessons from eosinophilic airway inflammation in the mouse.

Asthma is a chronic disorder of the airways characterized by variable airway narrowing, mucus hypersecretion, and infiltration of the airway wall with eosinophils. It is now believed that asthma is controlled by Th2 lymphocytes producing cytokines such as IL-4, IL-5, IL-9, and IL-13. Animal models of eosinophilic airway inflammation and airway hyperreactivity have been developed to study the contribution of cells or mediators in the pathogenesis of asthma. In this review, we discuss the role of antigen presenting cells, CD4(+) and CD8(+) T lymphocytes, B lymphocytes, NK cells, and mast cells in the induction and maintenance of eosinophilic airway inflammation, mucus hypersecretion, and airway hyperreactivity.

Administration, Inhalation↗