{'fraction_non_alphanumeric': 0.041901188242651655, 'fraction_numerical': 0.021263289555972485, 'mean_word_length': 5.926406926406926, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Augmentation of monocyte interleukin‐8 production by psoralen/UVA‐treated CD4+ T cells

Abstract: Treatment of cells with psoralen and ultraviolet A light (UVA) modulates their cytokine production. As extracorporeal photochemotherapy has been reported to induce cytokine production by monocytes, we quantified interleukin‐8 (IL‐8), a representative chemokine produced by monocytes, in culture supernatants from human peripheral blood mononuclear cells (PBMC) treated with 8‐methoxypsoralen (8‐MOP) and UVA. Lipopolysaccharide stimulated IL‐8 production in 8‐MOP‐phototreated PBMC more efficiently than those untreated or treated with 8‐MOP or UVA. More interestingly, when cultured with T‐cell‐stimulating anti‐CD3 and anti‐CD28 antibodies, 8‐MOP/UVA‐treated PBMC produced enhanced amounts of IL‐8 with an increased level of IL‐8 mRNA expression. Depletion of CD4 but not CD8 T cells from PBMC abrogated this augmented IL‐8 elaboration, and CD4 T cells per se secreted no substantial amount of IL‐8 even upon CD3/CD28 stimulation. Thus, 8‐MOP/UVA‐treated CD4 T cells stimulated monocytes to secrete IL‐8. The IL‐8 overproduction was induced by direct contact of monocytes with 8‐MOP/UVA‐treated CD4 T cells but not by cytokines from the treated CD4 T cells. These findings imply that in extracorporeal photochemotherapy, monocytes effectively produce IL‐8 by cell‐to‐cell contact with 8‐MOP/UVA‐treated malignant CD4 T cells. The augmentation of monocyte cytokine/chemokine production by 8‐MOP/UVA may be one of the mechanisms underlying the therapeutic efficacy of extracorporeal photochemotherapy.