PMID- 18797896 OWN - NLM STAT- MEDLINE DCOM- 20081211 LR - 20220409 IS - 1432-069X (Electronic) IS - 0340-3696 (Linking) VI - 300 IP - 10 DP - 2008 Nov TI - 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. PG - 551-9 LID - 10.1007/s00403-008-0886-6 [doi] AB - 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. FAU - Borghi, Alessandro AU - Borghi A AD - Department of Clinical and Experimental Medicine, Section of Dermatology, University of Ferrara, Via Savonarola 9, 44100 Ferrara, Italy. FAU - Fogli, Emanuela AU - Fogli E FAU - Stignani, Marina AU - Stignani M FAU - Melchiorri, Loredana AU - Melchiorri L FAU - Altieri, Ermete AU - Altieri E FAU - Baricordi, Olavio AU - Baricordi O FAU - Rizzo, Roberta AU - Rizzo R FAU - Virgili, Annarosa AU - Virgili A LA - eng PT - Journal Article DEP - 20080917 PL - Germany TA - Arch Dermatol Res JT - Archives of dermatological research JID - 8000462 RN - 0 (Antibodies, Monoclonal) RN - 0 (Antibodies, Monoclonal, Humanized) RN - 0 (Dermatologic Agents) RN - 0 (HLA Antigens) RN - 0 (HLA-G Antigens) RN - 0 (Histocompatibility Antigens Class I) RN - 130068-27-8 (Interleukin-10) RN - 83HN0GTJ6D (Cyclosporine) RN - LCH760E9T7 (Acitretin) RN - XX2MN88N5D (efalizumab) SB - IM MH - Acitretin/therapeutic use MH - Adult MH - Aged MH - Aged, 80 and over MH - Antibodies, Monoclonal/therapeutic use MH - Antibodies, Monoclonal, Humanized MH - Case-Control Studies MH - Cross-Sectional Studies MH - Cyclosporine/therapeutic use MH - Dermatologic Agents/therapeutic use MH - Female MH - Gene Frequency/genetics MH - Genotype MH - HLA Antigens/*blood MH - HLA-G Antigens MH - Histocompatibility Antigens Class I/*blood MH - Humans MH - Immune System/pathology/*physiopathology MH - Interleukin-10/*blood MH - Male MH - Middle Aged MH - Polymorphism, Genetic/genetics MH - Psoriasis/*blood/drug therapy/genetics MH - T-Lymphocytes/pathology MH - Young Adult EDAT- 2008/09/18 09:00 MHDA- 2008/12/17 09:00 CRDT- 2008/09/18 09:00 PHST- 2008/04/07 00:00 [received] PHST- 2008/08/21 00:00 [accepted] PHST- 2008/07/07 00:00 [revised] PHST- 2008/09/18 09:00 [pubmed] PHST- 2008/12/17 09:00 [medline] PHST- 2008/09/18 09:00 [entrez] AID - 10.1007/s00403-008-0886-6 [doi] PST - ppublish SO - Arch Dermatol Res. 2008 Nov;300(10):551-9. doi: 10.1007/s00403-008-0886-6. Epub 2008 Sep 17.