signals (such as IL-22) have been shown to correlate with the severity and chronicity of AD in addition to levels of CCL17, although the causal relationships between each of these other signals and CCL17 are not all yet known. Other signaling components, like TSLP, are induced by other lesional epidermal cells and directly upregulate CCL17 production. Clinically, CCL17 has recently shown promise as a useful biomarker for AD severity as well as efficacy of treatment. Historically, physicians have used mostly visual, qualitative evaluations of lesion progress, but using CCL17 to quantify AD has allowed for more precise and accurate records of progress (or regression) during treatment. In concert with this, proposed treatments for AD include topical regulation of CCL17. Especially for infantile AD, where prolonged AD has been linked to severe food allergies, early quantification and treatment is especially important. This treatment may take the form of small-molecule inhibition of CCL17-CCR4 binding, which inhibits recruitment of Th2 cells and subsequent development of lesions. Multiple sclerosis (and EAE) Multiple sclerosis (MS) (and the animal model EAE) are autoimmune diseases characterized in part by changes in the expression and regulation of CCL17 in cerebrospinal fluid. There is also evidence to suggest that certain SNPs in the CCL17 and CCL22 genes may raise the risk of MS for an individual. While type 2 helper T (Th2) cells are a key component of AD because they are localized to the skin through the CCL17-CCR4 interaction, memory Th17 cells seem to express high levels of CCR4 in both human and murine models of MS and are therefore likely candidates for study and therapy. Treatments of MS (such as natalizumab or methylprednisolone) seem to lower overall chemokine levels (notably including either CCL17 itself or factors that are known to induce CCL17 production) in addition to other purported primary functions. However, these findings are complicated by CCR4 up- and downregulation findings, which have sometimes seemed counter to the CCL17 localization pathways. Experimental explorations with CCL17-deficient mice have therefore counterintuitively given different information than experiments measuring CCR4 regulation for EAE. Other disorders Several other disorders are also correlated with high levels of CCL17 or use CCL17 to localize Th2 cells. CCL17 can act as an inflammatory agent or as a symptom, and in either case, disrupting or manipulating the expression or ligand binding offers a therapeutic target. And, regardless of therapeutic potential, it can be used as a