IL-17 and Neutrophil Mobilization in Lungs

This presentation summarizes clinical and immunological aspects of the T cell cytokine interleukin-17 (abbreviated IL-17 or IL-17A) in the context of neutrophilic inflammation in mammalian lungs.
There is increasing evidence that IL-17, the archetype of the six members of the IL-17 family of cytokines, coordinates the innate and adaptive components of host defence in the lungs of mammals [1-3]. Notably, IL-17 production may also occur in horses with recurrent airway obstruction (also named heaves) [4- 7]. IL-17 is a 35 kDa homo-dimeric cytokine and it can probably be produced by several types of immune cells, including a unique subset of memory T helper cells, named Th-17 [1-3, 8]. The IL-17 production seems to be restricted to relatively few local immune cells, whereas the IL-17 receptor (i.e. the IL17 A/C receptor complex) is widely distributed among structural organ cells [3, 8-12]. IL-17 receptors may act through Act 1, a recently discovered and potentially unique intracellular pathway, and in part through Jak; a wellknown intracellular pathway shared with many pro-inflammatory cytokines [10, 13].
By releasing IL-17, key immune cells orchestrate the local accumulation and activity of neutrophils through the induced release of C-X-C chemokines, colony-stimulating factors and IL-6 [2, 3, 14]. IL-17-producing cells seem to be involved not only in host defence against bacteria in the lungs, but also in host defence against certain fungi [15]. Moreover, local IL-17 is increased in several chronic inflammatory disorders in human lungs, including severe asthma and cystic fibrosis [3, 8, 10]. There is also supportive data showing IL-17 mRNA in BAL cells and bronchial tissue from horses with heaves [4, 7]. […]