CCL17 will also activate tumor-infiltrating lymphocytes tumors. For many cancers, the more CCL17 in the area, the better the prognosis is for cancer survival or recovery. Inflammation Like many cytokines, CCL17 is inflammatory, so while it plays a largely helpful role in attacking cancers, it can induce inflammatory diseases, including allergic skin diseases. Because of its inflammatory effects, much of the medical research is on methods to mitigate CCL17. Neutralizing CCL17 with monoclonal antibodies has been shown to relieve inflammatory arthritis and osteoarthritis. Topical steroids have been found to be an effective tool in normalizing levels of CCL17. Autoimmunity CCL17 is known to help leukocytes (and especially eosinophils) target their response to skin-located pathogens. This often occurs through the CCL17-CCR4 interaction on type 2 T helper cells, which then secrete a variety of interleukins. Direct interactions between CCL17 and eosinophils has been observed but not well defined. However, overexpressed CCL17 has been linked to atopic dermatitis (eczema) and multiple sclerosis, among other autoimmune diseases. Studies have shown that children with allergies and atopic dermatitis have higher quantiles of CCL17 compared to children without allergies. As such, therapeutic approaches involving CCL17 regulation have shown some success in several cases. This intervention often involves interfering with CCR4 through monoclonal antibody treatment (such as mogamulizumab). Another option is small-molecule interaction with CCR4, which has not yet had any clinical success. Atopic dermatitis (eczema) Researchers have found that type 2 helper-T cells in lesions of atopic dermatitis (AD) express more IL-4 and IL-13 than unaffected Th2 cells. Dendritic cells respond to IL-4 and IL-13 by secreting CCL17 (as well as CCL18 and CCL22), especially in "barrier-disrupted" skin (such as lesional skin). Because CCL17 is a key attractant for Th2, this creates a cycle of Th2 recruitment, IL-4 and IL-13 signaling, dendritic cell secretion of CCL17, and further recruitment of Th2 cells. Severity of AD is therefore correlated with concentration of CCL17 and CCL22 in both the blood serum and interstitial fluid of pediatric and adult patients with either acute or chronic AD. Because Th2 cells are present at elevated levels during pregnancy, a buildup of CCL17 in umbilical cord blood may summon more Th2 cells, causing the aforementioned positive feedback loop. This is correlated with a higher likelihood of developing AD (and other allergic diseases) in infants (including for mothers without AD), especially for the first two years of infancy. In adult patients, other