INTRODUCTION
In 1986, Mosmann and Coffman described two immunologic pathways using murine models. They discovered that the CD4+ T helper (Th) lymphocytes differentiate into two subtypes defined by their function and cytokines.1 Interleukin 12 (IL-12) and Interferon-y (INF-y) stimulate Th1, which is responsible for intracellular pathogen clearance and an inflammatory response. The stimulation of Th2 is induced by IL-4 and controls humoral response and extracellular pathogens. Both pathways (Th1 and Th2) potentiate their own expression and antagonize each other, leading to mutual exclusion.2Later on, the idea that Th1 cells with certain specificity for autoantigens that produce IFN-y introduced the possibility that Th1 cells were autopathogenic and required for the induction of organ-specific autoimmunity. This was based on animal model studies where the expression of INF-y in target tissue correlated with clinical signs of collagen-induced arthritis (CIA) and experimental autoimmune encephalomyelitis (EAE). Also, a polyclonal antibody for IL-12 as a therapy was effective against CIA and EAE. In later animal model studies, it was demonstrated that IL-12 and INF-y deficient mice were not protected against these diseases; instead they were susceptible to more severe forms. These findings indicated that another group of cells different to Th1 were necessary to develop organ-specific autoimmune diseases.2,3In homologous sequence chain studies of IL-6 subfamilies it was discovered that the subunit p19, which forms heterodimers with p40 to form IL-12, was shared by a new cytokine which they called IL-23. Taking this in consideration, an effective treatment would need to target the subunit p40 to affect the development of EAE, since IL-23 and not IL-12 is the determinant for the development of this disease.4 It was then described that IL-23 had a role in Th17 differentiation as well as IL-17 production by leucocytes like macrophages, neutrophils and mastocytes, along with the development of T CD4+ IL-17 producing cells. The discovery of this new pathway IL-23/17 opened the door to a better understanding of the immune system.5
Interleukin 17
The IL-17 is a homodimeric (or heterodimeric) glycoprotein (35kDa) that works like a bridge between the innate and adaptive immunity.6,7 It plays an important role defending against extracellular pathogens and promoting inflammatory pathologies.8 Six members have been described as part of the family of IL-17: IL-17A, B, C, D, E (also named IL-25), and F. IL-17A has been identified as the most important pro-inflammatory cytokine among the IL-17 family when bound to its receptor. In vivo, IL-17A can be found as a homodimeric glycoprotein (35kDa) made of 2 IL-17A,6 which binds with great affinity to its
