Cytokines in XXXX .

@entity225 @entity4047 @entity39 @entity5 @entity565 @entity8923 @entity379 @entity3646
The airway inflammation underlying @entity565 is regulated by a network of mutually interacting cytokines. The exact functional role of each individual cytokine in the pathogenesis of the disease remains to be fully established. Type 2 T-helper cells are currently considered to play a crucial role in this process. In vivo animal data suggest a sequential involvement of @entity3646 and @entity225 in the induction of allergen-induced airway changes. The potential role of other type 2 T-helper cell-like cytokines in @entity565 is increasingly being recognized. In particular, @entity3646 and -13 display a large degree of redundancy. Whereas @entity3646 seems to be crucial in the primary allergen sensitization process, @entity4047 might be more important during secondary exposure to aerosolized allergen. Animal models also indicate that T-cell-derived cytokine production, rather than eosinophil influx or immunoglobulin-E synthesis, is causally related to altered airway behaviour. An important aspect when evaluating the functional role of cytokines in a complex disease such as @entity565 is the interaction with other cytokines in the microenvironment. Increased expression of pro-inflammatory cytokines such as @entity5 @entity39 factor-alpha can further enhance the inflammatory process, and is increasingly linked to disease severity. In addition, decreased expression of immunoregulatory cytokines, including interleukin-12, @entity8923 or @entity379 could also strengthen the type 2 T-helper cell-driven inflammatory process.
