Photopheresis up-regulates CD36 on monocytes and reduces CD25(+) and CD28(+) T cell numbers

Extracorporeal photopheresis (ECP) is an effective treatment for some malignant T cell proliferations and disorders associated with pathogenic T cell activation. ECP induces apoptosis in lymphocytes and up-regulates the antigen-processing ability of monocytes. Recently, it has been proposed that the anti-tumour response, generated by ECP, can be enhanced by prolonging the co-culture of the ECP-treated lymphocytes and monocytes prior to re-infusion. However, early markers of lymphoid apoptosis and changes in cytokine secretion have been observed immediately following ECP. This study aimed to determine the rapid effects of ECP on significant markers associated with antigen presentation.

Pre- and post-ECP samples, from 11 chronic graft versus host disease (cGvHD) and 3 cutaneous T cell lymphoma (CTCL) patients, were tested. The monocytes were evaluated for CD36 and CD91 expression, whilst the number of T cells positive for CD25, CD28, CD62L, CD152 and CD154 were determined. The pre- and post-ECP samples were compared statistically to determine change and both pre- and post-samples were compared to age/sex-matched controls.

Monocyte expression of CD36 increased to normal immediately post-ECP in both patient groups, whilst the percentage of CD25(+) and CD28(+) T cells fell significantly in the cGvHD cohort following ECP.

CD36 is an important receptor for the uptake of apoptotic material and its up-regulation would be beneficial in the antigen-processing mechanism proposed for ECP. No enhancement in markers of T cell activation would indicate that ECP-treated lymphocytes play no direct role in the proposed cytotoxic response. However, reduction in CD25 and CD28 may represent a mechanism beneficial in disease states with excess T cell activation.