Chemokines are a type of cytokine that attract white blood cells to sites of inflammation or disease.
[5] CCL17 is expressed constitutively in the thymus, but only transiently in phytohemagglutinin-stimulated peripheral blood mononuclear cells.
[13] It can be detected by immunohistochemistry in >90% of cases in a diagnostic setting and is highly specific within B cell derived cancers.
[14] CCL17 is mainly responsible for the presence of large amounts of T-helper and T-regulatory cells in the tumor microenvironment, which is considered a hallmark of Hodgkin lymphoma.
[15] Levels of CCL17 in serum are ~400 times higher in Hodgkin lymphoma patients than in healthy controls and are strongly associated with tumor volume, disease stage, and response to therapy.
[16][17] [18][19][20][21][22][23][24] Its levels are increasing already several years prior to symptoms and diagnosis in many Hodgkin lymphoma patients.
[27] However, overexpressed CCL17 has been linked to atopic dermatitis (eczema) and multiple sclerosis, among other autoimmune diseases.
Other signaling components, like TSLP, are induced by other lesional epidermal cells and directly upregulate CCL17 production.
[31] Clinically, CCL17 has recently shown promise as a useful biomarker for AD severity as well as efficacy of treatment.
[28] 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.
[28] 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.
[28] Experimental explorations with CCL17-deficient mice have therefore counterintuitively given different information than experiments measuring CCR4 regulation for EAE.
[27] 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.