title: Enhanced proliferation and activation of peripheral blood mononuclear cells in patients with psoriasis vulgaris mediated by streptococcal antigen with bacterial DNA.
abstract: Streptococcal infection is believed to have an intimate relationship with psoriasis, although the pathogenic role of streptococcal DNA is not fully understood. To gain a clearer understanding of these dynamics, we investigated the effect of streptococcal DNA on lymphocyte proliferation and activation as well as cytokine secretion in psoriasis. Peripheral blood mononuclear cells (PBMCs) from psoriatic patients had higher proliferative responses upon stimulation by streptococcal antigen (SA) when compared with those from healthy individuals. Strikingly, this enhanced proliferation of PBMCs was attenuated after administration of SA treated with DNase-I. In addition, CD69 expression levels on T cells, including skin-homing lymphocyte cutaneous lymphocyte-associated antigen positive T cells, and IFN-alpha secretion by PBMCs were also attenuated in patients after stimulation with SA without nucleic acid (non-nucleic acid SA, non-NASA) compared with stimulation with untreated SA. However, activation marker CD86 expression levels on B cells as well as the secretion of IFN-gamma and tumor necrosis factor (TNF)-alpha following stimulation with SA or non-NASA were not significantly altered. Interestingly, the attenuated T-cell activation and IFN-alpha secretion in psoriatic patients could be reconstituted when stimulated by non-NASA combined with synthetic CpG-A, but not when combined with synthetic CpG-B. This study demonstrates the integral function of SA, particularly streptococcal DNA, in the pathogenesis of psoriasis.
authors.affiliation: Department of Dermatology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
authors.forename: Yi-Hua
authors.initials: YH
authors.lastname: Cai
authors.forename: Zhi-Yong
authors.initials: ZY
authors.lastname: Lu
authors.forename: Ruo-Fei
authors.initials: RF
authors.lastname: Shi
authors.forename: Feng
authors.initials: F
authors.lastname: Xue
authors.forename: Xiao-Ying
authors.initials: XY
authors.lastname: Chen
authors.forename: Meng
authors.initials: M
authors.lastname: Pan
authors.forename: Wei-Ru
authors.initials: WR
authors.lastname: Yuan
authors.forename: Han
authors.initials: H
authors.lastname: Xu
authors.forename: Wei-Ping
authors.initials: WP
authors.lastname: Li
authors.forename: Jie
authors.initials: J
authors.lastname: Zheng
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial / Q000276:immunology / Q000494:pharmacology; D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D001402:B-Lymphocytes / Q000166:cytology / Q000276:immunology* / Q000382:microbiology; D002455:Cell Division / Q000187:drug effects / Q000276:immunology; D002648:Child; D004269:DNA, Bacterial / Q000276:immunology; D003850:Deoxyribonuclease I / Q000494:pharmacology; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D037181:Lectins, C-Type; D008213:Lymphocyte Activation / Q000276:immunology; D008875:Middle Aged; D009838:Oligodeoxyribonucleotides / Q000494:pharmacology; D011565:Psoriasis / Q000276:immunology* / Q000473:pathology*; D013290:Streptococcal Infections / Q000276:immunology; D013291:Streptococcus / Q000235:genetics / Q000276:immunology*; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology* / Q000382:microbiology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D055815:Young Adult; D000099192:CD69 Antigens
chemical_list: D000942:Antigens, Bacterial; D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D004269:DNA, Bacterial; D003850:Deoxyribonuclease I; D007371:Interferon-gamma; D037181:Lectins, C-Type; D009838:Oligodeoxyribonucleotides; D014409:Tumor Necrosis Factor-alpha; D000099192:CD69 Antigens; C408982:CPG-oligonucleotide