title: Soluble human leukocyte antigen-G and interleukin-10 levels in plasma of psoriatic patients: preliminary study on a possible correlation between generalized immune status, treatments and disease.
abstract: Human leukocyte antigen (HLA)-G is a non-classical HLA class I molecule that exerts a generalized immunosuppressive action. A deficit in membrane bound and soluble HLA-G levels seems to cause a defective control on immune responses and trigger off several autoimmune diseases. As psoriasis is considered an autoimmune disease, lower levels of soluble HLA-G (sHLA-G) might be expected in psoriatic patients than in healthy controls. The aims of this descriptive study were: (1) to evaluate whether sHLA-G levels are different in psoriatic patients compared to controls; (2) to compare sHLA-G levels between groups of patients treated with different therapies; (3) to evaluate whether any differences found in HLA-G expression could be related to a genetic control. Peripheral blood samples were investigated for sHLA-G and IL-10 levels and for HLA-G 14 bp polymorphism in 65 patients with moderate-to-severe plaque psoriasis treated with systemic drugs or with topical or physical treatments and in controls. Significantly lower plasma levels of both sHLA-G and IL-10 were found in psoriatic group compared to controls and in local treated patients in comparison with systemic treated patients. These findings could indicate that low sHLA-G levels may contribute to susceptibility to psoriasis. Absence of differences in HLA-G 14 bp allele and genotype frequencies between psoriatic patients and controls and between patients following different treatments seems to exclude genetic bases of sHLA-G levels. It could be speculated that therapeutics antagonizing systemic T helper 1 activation may induce sHLA-G secretion via an IL-10-dependent pathway.
authors.affiliation: Department of Clinical and Experimental Medicine, Section of Dermatology, University of Ferrara, Via Savonarola 9, 44100 Ferrara, Italy.
authors.forename: Alessandro
authors.initials: A
authors.lastname: Borghi
authors.forename: Emanuela
authors.initials: E
authors.lastname: Fogli
authors.forename: Marina
authors.initials: M
authors.lastname: Stignani
authors.forename: Loredana
authors.initials: L
authors.lastname: Melchiorri
authors.forename: Ermete
authors.initials: E
authors.lastname: Altieri
authors.forename: Olavio
authors.initials: O
authors.lastname: Baricordi
authors.forename: Roberta
authors.initials: R
authors.lastname: Rizzo
authors.forename: Annarosa
authors.initials: A
authors.lastname: Virgili
mesh_terms: D017255:Acitretin / Q000627:therapeutic use; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D016572:Cyclosporine / Q000627:therapeutic use; D003879:Dermatologic Agents / Q000627:therapeutic use; D005260:Female; D005787:Gene Frequency / Q000235:genetics; D005838:Genotype; D006680:HLA Antigens / Q000097:blood*; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I / Q000097:blood*; D006801:Humans; D007107:Immune System / Q000473:pathology / Q000503:physiopathology*; D016753:Interleukin-10 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic / Q000235:genetics; D011565:Psoriasis / Q000097:blood* / Q000188:drug therapy / Q000235:genetics; D013601:T-Lymphocytes / Q000473:pathology; D055815:Young Adult
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D003879:Dermatologic Agents; D006680:HLA Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I; D016753:Interleukin-10; D016572:Cyclosporine; D017255:Acitretin; C472181:efalizumab