Human T cell leukemia virus type-I (HTLV-I) is the causal virus for adult T cell leukemia (ATL) and HTLV-I-related myelopathy (HAM). In Okinawa islands located at the subtropical zone, the incidence rate of ATL is more than two times higher than other areas of Japan. Besides, the amounts of UV-B irradiation in Okinawa are about twice as much as any other areas of Japan throughout a year.
We assume that some sort of environmental factors, including UV exposure, can contribute to the oncogenic process of ATL through the survival of HTLV-I infected cells. In this study, we confirmed that PGE2 secreted by keratinocytes after the exposure to UV-B could induce the expression of co-inhibitory molecule:PD-L1, in HTLV-I infected T cell lines, 026i, 056i, ILT-H2. The supernatants of HaCaT cells after UV-B (50J/㎡2) irradiation enhanced the expression of PD-L1 in those cells.
We also confirmed that PGE2 (14nM) alone could enhance the expression of Tax and PD-L1 as 1.3 times to 3 times as a vehicle, and that these enhancements were completely blocked by the specific EP4 antagonist:L-161,982, in those cells. In RNA microarray analysis, PGE2 enhanced the expression of EBI3 and CCR6 as 3.09 and 5.91 fold changes. From these results, we consider that the sustained UVB exposure can contribute to the survival of HTLV-I infected T cells through the induction of co-inhibitory molecule like PD-L1, and EBI3: β subunit of IL-35. 
ATL often involve the lymph node and occasionally gastrointestinal lesions. We think that the induced CCR6 expression by PGE2 at skin can trigger the malignant alteration of lymph node and gastrointestinal lesions  in addition to skin lesion. We think that strong sunshine against HTLV-I carrier persons in the subtropical area can promote and result in the development of ATL.

Sustained UV-B irradiation can impair the host immune-surveillance and exacerbate the cutaneous,  gastrointestinal and lymph node lesions through the induction of PD-L1,  EBI3 and CCR6 expression.