Th-17 cells in the lungs?

Abstract

Naive CD4 cells are capable of integrating signals from antigen-activated cells of the innate immune system and differentiating into effector CD4 cells, also termed T helper (Th) cells. According to the traditional paradigm explaining adaptive CD4 cell responses, there are two subsets of Th cells: the Th-1 and Th-2 subset. Each of these subsets undergoes a distinct differentiation pathway (a pathway that is characterized by a unique profile of cytokine production and has specific immunoregulatory functions). However, recent studies in mouse models have forwarded evidence of a third subset of Th cells: the Th-17 subset. As indicated predominantly in studies on mice, the Th-17 subset is characterized by an ability to produce the neutrophil-mobilizing cytokine IL-17 in response to stimulation with the cytokine IL-23, an IL-12-related cytokine released from antigen-presenting cells. There is now a growing body of evidence from animal models that the Th-17 subset plays an important role in host defence in the lungs and other organs. Altered IL-17 levels have also been demonstrated in human patients with asthma, exacerbations of cystic fibrosis or following lung transplantation. There is now also evidence that the Th-17 subset is functionally distinct from the Th-2 subset but little is known of the functional inter-relationship between the Th-1 and Th-17 cell subsets; this is particularly true in human lungs. It has been proposed that the Th-17 subset plays a unique role by linking the arms of innate and adaptive immunity. Thus, an improved understanding of the human correlate to the Th-17 subset may reveal new targets for pharmacotherapy against lung disorders that are characterized by aberrant innate responses in host defense.

Keywords::

• host defence
• innate immunity
• IL-17
• IL-23
• lung disease
• macrophages
• neutrophils
• Th-17 cells

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.