CCL1 was initially identified as a secreted protein derived from activated T cells. The CCL1/CCR8 axis is involved in the recruitment of Th2 effector cells in vivo to sites of allergic mucosal inflammation; as a result, there is an increase of CCR8+ CD4 T cell numbers in allergic asthma and a higher concentration of CCL1 in bronchoalveolar lavage of asthmatic patients compared with normal controls. In addition, high levels of CCL1 have been detected in the serum of patients with atopic dermatitis. CCL1 is constitutively expressed in normal skin, and CD8 and CD4 CCR8+ cells have been isolated from normal skin. Therefore, it has been suggested that CCL1/CCR8 play a role in skin immunosurveillance. In addition, a more recent publication showed that CCL1 transcript is upregulated in CD4 converted to Tregs by TGF-beta in vitro, and this transcriptional upregulation is reversed by IL-6. This data suggests that CCL1 plays a role in Treg conversion. Also, antibodies against CCL1 inhibit the suppressive function of Tregs. Furthermore, the antitumor effect of CpG-ODN plus anti-CCL1 in BALB-neuT mice suggest that neutralization of CCL1 can be used as an adjuvant to antitumor immunotherapy.