Like Th9 cells, Th22 cells participate predominantly in barrier immunity, stimulating the production of anti-microbial molecules by epithelial and mucosal cells. Cells driving its differentiation (through TGF-α and IL-6) are also mainly innate immune cells. IL22 is its main mediator (also TNFα), which is also produced by Th17 cells. As such, its effects most resemble Th17's, albeit its more "pathogenic" form.
In health, Th22 protects against skin, airway and gut extracellular bacteria. It is anti-apoptotic, promoting regeneration and repair. It's "unbridled exuberance" is implicated in conditions like Psoriasis, Ankylosing Spondylitis, Crohn's Disease and colonic cancer. Its dormant skin localisation may even retain immune memory within pathological lesions.
At least 2 anti-IL23 biologics are in mid-to-late stage trials, possibly yielding greater efficacy in Psoriasis and Crohn's Disease. This may partly be due to its immediate upstream control of both IL22 and IL17.
"IL-22 induces the production of various antimicrobial peptides from epithelial cells.2 S100A8 and S100A9 are calcium-binding proteins produced by neutrophils, monocytes, and epithelial cells under inflammatory conditions.21 S100A8 and S100A9 are components of the heterodimeric protein calprotectin. An increased expression of S100A8 and S100A9 is associated with human ulcerative colitis and CD..."
Now you know what Calprotectin is, and why it serves as a surrogate marker of gut inflammation.