Reduced innate interleukin-22 (IL-22) in genes. production of IL-22 and/or IL-17) (Sonnenberg et al., 2011; Tumanov et al., 2011; Wang et al., 2010), and thus coevolution of two systems might be a fail-safe mechanism for implementing redundancy into host immunity to certain infections, especially at mucosal surfaces. Consistent with this notion, although and 3AC enteropathogenic infections (Mangan et al., 2006). Most recently, it has been reported that ILC-produced IL-22 is essential for clearance of in the intestines (Sonnenberg et al., 2011; Zheng et al., 2008). Intriguingly, even in the lymphocyte-replete hosts, mice lacking RORt+ ILCs died from contamination (Sonnenberg et al., 2011). An intact ILC compartment is also important for preventing peripheral dissemination of commensal bacteria (i.e., species) that normally reside in host lymphoid tissues (Sonnenberg et al., 2012). These data spotlight an Rabbit Polyclonal to EPS15 (phospho-Tyr849) essential role for ILCs in host immunity against 3AC overt pathogens and opportunistic commensals. Segmented filamentous bacteria (SFB), a type of intestinal commensal found in mice, have been shown to be important for in vivo Th17 induction (Gaboriau-Routhiau et al., 2009; Ivanov et al., 2009). Mice lacking SFB show a substantial reduction in Th17 cells in the small intestine, and monocolonization of gnotobiotic mice with SFB can restore intestinal Th17 cells (Ivanov et al., 2009). Although microbiota can promote or suppress IL- 22 production by group 3 ILCs (Sanos et al., 2009; Satoh- Takayama et al., 2008; Sawa et al., 3AC 2011), the development of group 3 ILCs seems to be impartial of gut flora or SFB (Reynders et al., 2011; Sawa et al., 2010). The impact of group 3 ILCs on gut flora, especially commensal bacteria, however, remains to be elucidated. Recent data suggest a similarity between ILCs and T helper cells in transcriptional regulation (Zhou, 2012). T-bet, a Th1- cell-lineage transcription factor, has been shown to be important for IFN- production by certain ILCs (Bernink et al., 2013; Buonocore et al., 2010; Klose et al., 2013; Powell et al., 2012; Scium et al., 2012). Gata3, a key transcription factor for Th2 cells, is crucial for ILC2 development and function (Hoyler et al., 2012; Mj?sberg et al., 2012). RORt, a common transcription factor shared by Th17 cells and group 3 ILCs, is not only important for Th17 cell differentiation but is also essential for group 3 ILC development (Eberl et al., 2004; Ivanov et al., 2006). Aryl 3AC hydrocarbon receptor (Ahr) is usually a ligand-dependent transcription factor best known for mediating the carcinogenicity of a family of environmental contaminants (i.e., xenobiotic ligands). Recent data suggest that Ahr also plays an important physiological role in the immune system (Stockinger et al., 2011). The expression of Ahr is usually important for the maintenance, survival, and function of group 3 ILCs (Kiss et al., 3AC 2011; Lee et al., 2012; Qiu et al., 2012). Ahr cooperates with RORt to induce the transcription of IL-22, which is essential for the clearance of contamination (Qiu et al., 2012). Although Ahr can be indicated by both intestinal Th17 cells and group 3 ILCs and promotes in vitro Th17 cell differentiation (i.e., enhances IL-17 manifestation in Compact disc4+ T cells) (Kimura et al., 2008; Quintana et al., 2008; Veldhoen et al., 2008), it continues to be to be established whether Ahr is important in the rules of in vivo Th17 cell reactions specifically in the gut, a spot where Th17 group and cells 3 ILCs are both prominently within the steady-state physiological circumstances. The crosstalk between ILCs as well as the adaptive disease fighting capability.