IL-8 (CXCL8), which leads to neutrophil production and recruitment. In this way, Th17 cell lineage appears to be one of the three major subsets of effector T cells, as these cells are involved in regulation of neutrophils, while Th2 cells regulate eosinophils, basophils and mast cells, and Th1 cells regulate macrophages and monocytes. Thus, three T helper cell subsets are able to influence the myeloid part of the immune system, largely responsible for innate defense against pathogens. Treg17 cells with regulatory phenotype with in vivo immune-suppressive properties in the gut have also been identified as rTh17 cells. Treg17 cells produce IL-17 and IL-10 and low level of IL-22 and suppress autoimmune and other immune responses. CD4+ T cells polarized with IL-23 and IL-6 are pathogenic upon adoptive transfer in type 1 diabetes while cells polarized with TGF-beta and IL-6 are not pathogenic., The intracellular aryl hydrocarbon receptor (AhR), which is activated by certain aromatic compounds, is specifically expressed in Treg17 cells. These cells are regulated by IL-23 and TGF-beta. The production of IL-22 in this subset of Th17 cells is regulated by AhR and Treg17 cells are depend on activation of the transcription factor Stat3. In a steady state, TGF-beta and AhR ligands induce low expression of IL-22 along with high expression of AhR, c-MAF, IL-10, and IL-21 that might play a protective role in cell regeneration and host microbiome homeostasis. Th17 cells mediate the regression of tumors in mice, but were also found to promote tumor formation induced by colonic inflammation in mice. Like other T helper cells, Th17 cells closely interact with B cells in response to pathogens. Th17 cells are involved in B cell recruitment through CXCL13 chemokine signaling, and Th17 activity may encourage antibody production. Treg17 cells regulate the function of Th17 cells that are important role in the host defense against fungal and bacterial pathogens and participate in the pathogenesis of multiple inflammatory and autoimmune disorders. Selective deletion of Stat3 caused spontaneous severe colitis because of the lack of Treg17 cells and increase in pathogenic Th17 cells. The mechanism of Treg17 cell action is expression of chemokine receptor CCR6, which facilitates trafficking into areas of Th17 inflammation. This is also seen in human disease such glomerulonephritis (GN) in the kidney. Conversion of pathogenic Th17 cells in vivo at the conclusion of an inflammatory disease process by TGF-β results in the generation of Treg17 like cells.