Effector CD4+ T cells of the T_H17-type coordinate inflammatory episodes, primarily at mucosal surfaces, through secreted effector cytokines. When improperly regulated these cytokines have the capacity to initiate or contribute to inflammation-mediated pathology in a variety of organ systems. Indeed T_H17 cells have been implicated in numerous autoimmune and autoinflammatory disorders in mice and men, including multiple sclerosis, psoriasis, rheumatoid arthritis, the inflammatory bowel diseases, and uveitis, to name a few. As such, T_H17-associated factors are currently prime targets for therapeutic intervention.

Among the well-studied T_H17-associated factors are several interleukins, including IL-17 family proteins and IL-22. These cytokines are critical for proper host defense against Gram-positive and Gram-negative bacteria as well as parasitic and fungal pathogens. It is now widely appreciated, however, that these cytokines are multifunctional and influence a variety of distinct biological processes. In addition to eliciting antimicrobial peptide production and recruiting neutrophils and other immune cells to an inflammatory site, these cytokines modulate myeloid, lymphoid, and epithelial cell function, vascular remodeling, and even granulopoiesis.

We are interested in articles that highlight the ways in which these factors contribute to the initiating as well as resolving phases of inflammation, mediating host control of invading pathogens while coordinating mucosal healing and tissue repair.

We encourage investigators to submit original research manuscripts as well as review articles on all aspects of IL -17 and IL-22 biology; we are particularly interested in articles that focus on the regulatory nature of these cytokines during inflammation. Potential topics include, but are not limited to:

• The role of T_H17-associated cytokines in the inflammatory bowel diseases (IBDs)
• The contribution of T_H17-associated cytokines to autoimmune disease processes in rheumatoid arthritis, multiple sclerosis, and others
• Defining the contribution of IL-17 proteins in inflammatory episodes in skin
• Identifying key factors that modulate T_H17 cell pathogenicity
• The impact of non-T_H17 cell sources of T_H17-associated cytokines in mucosal immunity and host defense (i.e., gamma delta T cells, innate lymphoid cells, etc.)
• The role of T_H17-associated cytokines in the progression to neoplasia
• Novel strategies to alter T_H17 cell function for clinical benefit

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/jir/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/jir/tchd/ according to the following timetable: