title: Biologic therapy improves psoriasis by decreasing the activity of monocytes and neutrophils.
abstract: Therapy with monoclonal antibodies to tumor necrosis factor (TNF)-α and the interleukin (IL)-12/23 p40 subunit has significantly improved the clinical outcome of patients with psoriasis. These antibodies inhibit the effects of the target cytokines and thus the major concern during their use is the induction of excessive immunosuppression. Recent studies evaluating the long-term efficacy and safety of biologic therapy in psoriasis have shown no significant appearance of serious adverse effects including infections and malignancies. However, the immunological consequence and the mechanism by which the blockade of a single cytokine by biologics can successfully control the activity of psoriasis remain unclear. In the current study, we investigated the effect of biologic therapy on cytokine production of various lymphocytes and on the activity of monocytes and neutrophils in psoriatic patients. Neutrophils, monocytes and T cells were purified from heparinized peripheral venous blood by Ficoll density gradient centrifugation, and γ-interferon, TNF-α and IL-17 production from lymphocytes was measured by flow cytometer. The activation maker of neutrophils and the activated subsets of monocytes were also analyzed. Biologic therapy induced no significant changes in the cytokine production by lymphocytes from the skin and gut-homing T cells. However, neutrophil activity and the ratio of activated monocyte population increased in severely psoriatic patients were normalized in psoriatic patients receiving biologic therapy. The present study showed that biologic therapy ameliorates clinical symptoms and controls the immune response in patients with psoriasis.
authors.affiliation: Department of Dermatology, Mie University, Graduate School of Medicine, Tsu, Japan.
authors.forename: Keiichi
authors.initials: K
authors.lastname: Yamanaka
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Umezawa
authors.forename: Akisa
authors.initials: A
authors.lastname: Yamagiwa
authors.forename: Hidehisa
authors.initials: H
authors.lastname: Saeki
authors.forename: Makoto
authors.initials: M
authors.lastname: Kondo
authors.forename: Esteban C
authors.initials: EC
authors.lastname: Gabazza
authors.forename: Hidemi
authors.initials: H
authors.lastname: Nakagawa
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Mizutani
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D001688:Biological Products / Q000627:therapeutic use*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D005260:Female; D006801:Humans; D000069285:Infliximab; D007371:Interferon-gamma / Q000096:biosynthesis; D053762:Interleukin-12 Subunit p40 / Q000037:antagonists & inhibitors; D020381:Interleukin-17 / Q000096:biosynthesis; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D011565:Psoriasis / Q000276:immunology* / Q000628:therapy*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D000069549:Ustekinumab
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D001688:Biological Products; D053762:Interleukin-12 Subunit p40; D020381:Interleukin-17; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; D000069285:Infliximab; D000069549:Ustekinumab
keywords: infliximab; monocyte; neutrophil; psoriasis; ustekinumab