Psoriasis: from pathogenesis to novel therapeutic approaches.
暂无分享,去创建一个
[1] A. Blauvelt,et al. Circulating Th17, Th22, and Th1 cells are increased in psoriasis. , 2010, The Journal of investigative dermatology.
[2] K. Asadullah,et al. The Th17 cytokine IL‐22 induces IL‐20 production in keratinocytes: A novel immunological cascade with potential relevance in psoriasis , 2009, European journal of immunology.
[3] J. Dreiher,et al. Coeliac disease associated with psoriasis , 2009, The British journal of dermatology.
[4] S. Durham,et al. Th22 cells represent a distinct human T cell subset involved in epidermal immunity and remodeling. , 2009, The Journal of clinical investigation.
[5] L. Moreland,et al. Certolizumab pegol in active rheumatoid arthritis , 2009, Current rheumatology reports.
[6] J. Gudjonsson,et al. Psoriasis--as an autoimmune disease caused by molecular mimicry. , 2009, Trends in immunology.
[7] Frank O. Nestle,et al. Skin immune sentinels in health and disease , 2009, Nature Reviews Immunology.
[8] K. Gordon,et al. Long‐term efficacy of biologics in the treatment of psoriasis: what do we really know? , 2009, Dermatologic therapy.
[9] S. Chimenti,et al. Involvement of interleukin-21 in the epidermal hyperplasia of psoriasis , 2009, Nature Medicine.
[10] Courtney I. Jarvis,et al. Ustekinumab: Treatment of Adult Moderate-to-Severe Chronic Plaque Psoriasis , 2009, The Annals of pharmacotherapy.
[11] Andrew Blauvelt,et al. Th17 cytokines stimulate CCL20 expression in keratinocytes in vitro and in vivo: implications for psoriasis pathogenesis. , 2009, The Journal of investigative dermatology.
[12] A. Levine,et al. IL-6 Signaling in Psoriasis Prevents Immune Suppression by Regulatory T Cells1 , 2009, The Journal of Immunology.
[13] G. Chan,et al. Double-blind, placebo-controlled, dose-escalation study to evaluate the pharmacologic effect of CP-690,550 in patients with psoriasis. , 2009, The Journal of investigative dermatology.
[14] M. Gilliet,et al. Self-RNA–antimicrobial peptide complexes activate human dendritic cells through TLR7 and TLR8 , 2009, The Journal of experimental medicine.
[15] Pilar Romero,et al. IL‐17‐producing CD8+ T lymphocytes from psoriasis skin plaques are cytotoxic effector cells that secrete Th17‐related cytokines , 2009, Journal of leukocyte biology.
[16] D. West,et al. Monoclonal antibody-associated progressive multifocal leucoencephalopathy in patients treated with rituximab, natalizumab, and efalizumab: a Review from the Research on Adverse Drug Events and Reports (RADAR) Project. , 2009, The Lancet. Oncology.
[17] H. Spits,et al. Identification of a human helper T cell population that has abundant production of interleukin 22 and is distinct from TH-17, TH1 and TH2 cells , 2009, Nature Immunology.
[18] D. Jarrossay,et al. Production of interleukin 22 but not interleukin 17 by a subset of human skin-homing memory T cells , 2009, Nature Immunology.
[19] J. Schmitt,et al. Dovepress Open Access to Scientific and Medical Research Open Access Full Text Article Dovepress Targeted Treatment of Psoriasis with Adalimumab: a Critical Appraisal Based on a Systematic Review of the Literature , 2022 .
[20] F. Nestle,et al. The IL-23/Th17 axis in the immunopathogenesis of psoriasis. , 2009, The Journal of investigative dermatology.
[21] L. Kircik,et al. Anti-TNF agents for the treatment of psoriasis. , 2009, Journal of drugs in dermatology : JDD.
[22] A. Rivkin. Certolizumab pegol for the management of Crohn's disease in adults. , 2009, Clinical therapeutics.
[23] L. Boon,et al. Imiquimod-Induced Psoriasis-Like Skin Inflammation in Mice Is Mediated via the IL-23/IL-17 Axis1 , 2009, The Journal of Immunology.
[24] N. Yawalkar,et al. Increased expression of IL-12p70 and IL-23 by multiple dendritic cell and macrophage subsets in plaque psoriasis. , 2009, Journal of dermatological science.
[25] S. Chimenti,et al. Efficacy of Efalizumab in Psoriasis Patients Previously Treated with Tumour Necrosis Factor Blockers , 2009, Dermatology.
[26] R. Flavell,et al. How are T(H)1 and T(H)2 effector cells made? , 2009, Current opinion in immunology.
[27] D. Gladman,et al. Golimumab, a new human tumor necrosis factor alpha antibody, administered every four weeks as a subcutaneous injection in psoriatic arthritis: Twenty-four-week efficacy and safety results of a randomized, placebo-controlled study. , 2009, Arthritis and rheumatism.
[28] H. Volk,et al. IL-22 and IL-20 are key mediators of the epidermal alterations in psoriasis while IL-17 and IFN-γ are not , 2009, Journal of Molecular Medicine.
[29] Andrea W. M. Evers,et al. β-Defensin-2 Protein Is a Serum Biomarker for Disease Activity in Psoriasis and Reaches Biologically Relevant Concentrations in Lesional Skin , 2009, PloS one.
[30] Lisa C. Zaba,et al. Resident and "inflammatory" dendritic cells in human skin. , 2009, The Journal of investigative dermatology.
[31] Gonçalo Abecasis,et al. Deletion of the late cornified envelope LCE3B and LCE3C genes as a susceptibility factor for psoriasis , 2009, Nature Genetics.
[32] Pui-Yan Kwok,et al. Genomewide Scan Reveals Association of Psoriasis with IL-23 and NF-κB Pathways , 2008, Nature Genetics.
[33] F. Ginhoux,et al. Origin, homeostasis and function of Langerhans cells and other langerin-expressing dendritic cells , 2008, Nature Reviews Immunology.
[34] Lisa C. Zaba,et al. Th17 cytokines interleukin (IL)‐17 and IL‐22 modulate distinct inflammatory and keratinocyte‐response pathways , 2008, The British journal of dermatology.
[35] S. Echigo,et al. A polymer-type water-soluble peptidoglycan exhibited both Toll-like receptor 2- and NOD2-agonistic activities, resulting in synergistic activation of human monocytic cells , 2008, Innate immunity.
[36] Zhu Shen,et al. Dynamic frequency of CD4+CD25+Foxp3+ Treg cells in psoriasis vulgaris. , 2008, Journal of dermatological science.
[37] L. Cosmi,et al. Human interleukin 17–producing cells originate from a CD161+CD4+ T cell precursor , 2008, The Journal of experimental medicine.
[38] M. Gilliet,et al. Antimicrobial peptides and self-DNA in autoimmune skin inflammation. , 2008, Current opinion in immunology.
[39] Stefan Jenisch,et al. Polymorphisms of the IL12B and IL23R genes are associated with psoriasis. , 2008, The Journal of investigative dermatology.
[40] T. Macdonald,et al. Interleukin-21: a critical regulator of the balance between effector and regulatory T-cell responses. , 2008, Trends in immunology.
[41] M. Lebwohl,et al. Efficacy and safety of ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with psoriasis: 52-week results from a randomised, double-blind, placebo-controlled trial (PHOENIX 2) , 2008, The Lancet.
[42] A. Kimball,et al. Efficacy and safety of ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with psoriasis: 76-week results from a randomised, double-blind, placebo-controlled trial (PHOENIX 1) , 2008, The Lancet.
[43] D. Littman,et al. The differentiation of human TH-17 cells requires transforming growth factor-β and induction of the nuclear receptor RORγt , 2008, Nature Immunology.
[44] Sen Yang,et al. Fine Mapping of the Psoriasis Susceptibility Locus PSORS1 Supports HLA-C as the Susceptibility Gene in the Han Chinese Population , 2008, PLoS genetics.
[45] L. Fouser,et al. IL-22 is required for Th17 cell-mediated pathology in a mouse model of psoriasis-like skin inflammation. , 2008, The Journal of clinical investigation.
[46] A. Kimball,et al. Safety and efficacy of ABT-874, a fully human interleukin 12/23 monoclonal antibody, in the treatment of moderate to severe chronic plaque psoriasis: results of a randomized, placebo-controlled, phase 2 trial. , 2008, Archives of dermatology.
[47] Chen Dong,et al. T helper 17 lineage differentiation is programmed by orphan nuclear receptors ROR alpha and ROR gamma. , 2008, Immunity.
[48] A. Gottlieb,et al. A multicenter, open‐label study of repeat courses of intramuscular alefacept in combination with other psoriasis therapies in patients with chronic plaque psoriasis , 2008, The Journal of dermatological treatment.
[49] Lisa C. Zaba,et al. Amelioration of epidermal hyperplasia by TNF inhibition is associated with reduced Th17 responses , 2007, The Journal of experimental medicine.
[50] J. Kere,et al. The PSORS1 locus gene CCHCR1 affects keratinocyte proliferation in transgenic mice. , 2007, Human molecular genetics.
[51] D. Littman,et al. Transcriptional regulation of Th17 cell differentiation. , 2007, Seminars in immunology.
[52] I. Mellman,et al. Plasmacytoid dendritic cells sense self-DNA coupled with antimicrobial peptide , 2007, Nature.
[53] Khusru Asadullah,et al. Immunopathogenesis of psoriasis , 2007, Experimental dermatology.
[54] Kathleen M. Smith,et al. Development, cytokine profile and function of human interleukin 17–producing helper T cells , 2007, Nature Immunology.
[55] A. Menter,et al. Current and future management of psoriasis , 2007, The Lancet.
[56] Frank O. Nestle,et al. Sequence variants in the genes for the interleukin-23 receptor (IL23R) and its ligand (IL12B) confer protection against psoriasis , 2007, Human Genetics.
[57] J. Sprent,et al. Cytokines and T cell homeostasis. , 2007, Immunology letters.
[58] S. Chimenti,et al. A classification of psoriasis vulgaris according to phenotype , 2007, The British journal of dermatology.
[59] N. Van Rooijen,et al. Activated macrophages are essential in a murine model for T cell-mediated chronic psoriasiform skin inflammation. , 2006, The Journal of clinical investigation.
[60] M. Pasparakis,et al. Pathogenic role for skin macrophages in a mouse model of keratinocyte-induced psoriasis-like skin inflammation. , 2006, The Journal of clinical investigation.
[61] S. Chimenti,et al. Identical TCR β-Chain Rearrangements in Streptococcal Angina and Skin Lesions of Patients with Psoriasis Vulgaris1 , 2006, The Journal of Immunology.
[62] L. van der Fits,et al. Peptidoglycan and peptidoglycan‐specific Th1 cells in psoriatic skin lesions , 2006, The Journal of pathology.
[63] K. Asadullah,et al. IL‐22 regulates the expression of genes responsible for antimicrobial defense, cellular differentiation, and mobility in keratinocytes: a potential role in psoriasis , 2006, European journal of immunology.
[64] Stefan Jenisch,et al. Sequence and haplotype analysis supports HLA-C as the psoriasis susceptibility 1 gene. , 2006, American journal of human genetics.
[65] H. Young,et al. Impaired Langerhans cell migration in psoriasis , 2006, The Journal of experimental medicine.
[66] R. Steinman,et al. Increase in TNF-alpha and inducible nitric oxide synthase-expressing dendritic cells in psoriasis and reduction with efalizumab (anti-CD11a). , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[67] O. Arican,et al. Serum Levels of TNF-α, IFN-γ, IL-6, IL-8, IL-12, IL-17, and IL-18 in Patients With Active Psoriasis and Correlation With Disease Severity , 2005, Mediators of inflammation.
[68] C. Bernstein,et al. The clustering of other chronic inflammatory diseases in inflammatory bowel disease: a population-based study. , 2005, Gastroenterology.
[69] O. Boyman,et al. Plasmacytoid predendritic cells initiate psoriasis through interferon-α production , 2005, The Journal of experimental medicine.
[70] Matthew H Samore,et al. The Research on Adverse Drug Events and Reports (RADAR) project. , 2005, JAMA.
[71] S. Stevens,et al. Dysfunctional Blood and Target Tissue CD4+CD25high Regulatory T Cells in Psoriasis: Mechanism Underlying Unrestrained Pathogenic Effector T Cell Proliferation1 , 2005, The Journal of Immunology.
[72] J. Gudjonsson,et al. Peripheral blood T cell responses to keratin peptides that share sequences with streptococcal M proteins are largely restricted to skin‐homing CD8+ T cells , 2004, Clinical and experimental immunology.
[73] R. Trembath,et al. An update on the genetics of psoriasis. , 2004, Dermatologic clinics.
[74] A. Gottlieb,et al. Common clinical features and disease mechanisms of psoriasis and psoriatic arthritis , 2004, Current rheumatology reports.
[75] David J Margolis,et al. Psoriasis is common, carries a substantial burden even when not extensive, and is associated with widespread treatment dissatisfaction. , 2004, The journal of investigative dermatology. Symposium proceedings.
[76] Frank O. Nestle,et al. Spontaneous Development of Psoriasis in a New Animal Model Shows an Essential Role for Resident T Cells and Tumor Necrosis Factor-α , 2004, The Journal of experimental medicine.
[77] M. Dhodapkar,et al. Increased Expression of Interleukin 23 p19 and p40 in Lesional Skin of Patients with Psoriasis Vulgaris , 2004, The Journal of experimental medicine.
[78] D. Gladman,et al. CARD15: a pleiotropic autoimmune gene that confers susceptibility to psoriatic arthritis. , 2003, American journal of human genetics.
[79] B. Sigurgeirsson,et al. Streptococcal throat infections and exacerbation of chronic plaque psoriasis: a prospective study , 2003 .
[80] A. Andoh,et al. Increased expression of interleukin 17 in inflammatory bowel disease , 2003, Gut.
[81] W. Gulliver,et al. A randomized, double-blind, placebo-controlled phase III study evaluating efficacy and tolerability of 2 courses of alefacept in patients with chronic plaque psoriasis. , 2002, Journal of the American Academy of Dermatology.
[82] C. Griffiths,et al. Natural killer and natural killer-T cells in psoriasis , 2002, Archives of Dermatological Research.
[83] Y. Ishigatsubo,et al. Resolution of psoriasis following allogeneic bone marrow transplantation for chronic myelogenous leukemia: Case report and review of the literature , 2002, American journal of hematology.
[84] R. Trembath,et al. Family-based analysis using a dense single-nucleotide polymorphism-based map defines genetic variation at PSORS1, the major psoriasis-susceptibility locus. , 2002, American journal of human genetics.
[85] T. Ruzicka,et al. Role of Integrin αE(CD103)β7 for Tissue-Specific Epidermal Localization of CD8+ T Lymphocytes , 2001 .
[86] R. Vaughan,et al. Corneodesmosin Expression in Psoriasis Vulgaris Differs from Normal Skin and Other Inflammatory Skin Disorders , 2001, Laboratory Investigation.
[87] K. Takabayashi,et al. Increased interleukin-17 production in patients with systemic sclerosis. , 2000, Arthritis and rheumatism.
[88] S. Porcelli,et al. Overexpression of CD1d by Keratinocytes in Psoriasis and CD1d-Dependent IFN-γ Production by NK-T Cells1 , 2000, The Journal of Immunology.
[89] C. Wong,et al. Elevation of proinflammatory cytokine (IL-18, IL-17, IL-12) and Th2 cytokine (IL-4) concentrations in patients with systemic lupus erythematosus , 2000, Lupus.
[90] C. Albanesi,et al. Interleukin-17 is produced by both Th1 and Th2 lymphocytes, and modulates interferon-gamma- and interleukin-4-induced activation of human keratinocytes. , 2000, The Journal of investigative dermatology.
[91] A. Downs,et al. Exacerbation of psoriasis by interferon‐alpha therapy for hepatitis C , 2000, Clinical and experimental dermatology.
[92] J. Kere,et al. A candidate gene for psoriasis near HLA-C, HCR (Pg8), is highly polymorphic with a disease-associated susceptibility allele. , 2000, Human molecular genetics.
[93] P. Kivisäkk,et al. Interleukin-17 mRNA expression in blood and CSF mononuclear cells is augmented in multiple sclerosis , 1999, Multiple sclerosis.
[94] N. Yawalkar,et al. Expression of interleukin-12 is increased in psoriatic skin. , 1998, The Journal of investigative dermatology.
[95] A. Bowcock,et al. The genetics of psoriasis: a complex disorder of the skin and immune system. , 1998, Human molecular genetics.
[96] J. Snowden,et al. Development of psoriasis after syngeneic bone marrow transplant from psoriatic donor: further evidence for adoptive autoimmunity , 1997, The British journal of dermatology.
[97] A. Gottlieb,et al. PUVA bath therapy strongly suppresses immunological and epidermal activation in psoriasis: a possible cellular basis for remittive therapy , 1994, The Journal of experimental medicine.
[98] D. Duffy,et al. Psoriasis in Australian twins. , 1993, Journal of the American Academy of Dermatology.
[99] B. Weinshenker,et al. Remission of psoriatic lesions with muromonab-CD3 (orthoclone OKT3) treatment. , 1989, Journal of the American Academy of Dermatology.
[100] 古賀 千律子. Possible pathogenic role of Th17 cells for atopic dermatitis , 2011 .
[101] A. Boada,et al. A new era in the management of psoriasis? The biologics: facts and controversies. , 2010, Clinics in dermatology.
[102] J. Weinberg. Ustekinumab, a human interleukin 12/23 monoclonal antibody, for psoriatic arthritis: randomised, double-blind, placebo-controlled, crossover trial , 2010 .
[103] G. Plosker,et al. Efalizumab , 2009, American journal of clinical dermatology.
[104] L. Castelo-Soccio,et al. Long‐term efficacy of biologics in dermatology , 2009, Dermatologic therapy.
[105] G. Galbraith. Interleukin-22, a TH17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis , 2008 .
[106] B. Thiers. α1β1 integrin is crucial for accumulation of epidermal T cells and the development of psoriasis , 2008 .
[107] G. Galbraith. Identical TCR β-Chain Rearrangements in Streptococcal Angina and Skin Lesions of Patients with Psoriasis VulgarisDiluvio L, Vollmer S, Besgen P, et al (Ludwig-Maximilians-Univof Munich; Univ of Rome “Tor Vergata”; GSF-Research Ctr for Environment and Health, Munich) J Immunol 176:7104–7111, 2006§ , 2007 .
[108] L. Naldi,et al. Psoriasis and psoriatic arthritis: immunological aspects and therapeutic guidelines. , 2006, Clinical and experimental rheumatology.
[109] J. Pietrzyk,et al. Family studies in psoriasis , 2004, Archives of Dermatological Research.
[110] J. Voorhees,et al. Kinetics and regulation of human keratinocyte stem cell growth in short-term primary ex vivo culture. Cooperative growth factors from psoriatic lesional T lymphocytes stimulate proliferation among psoriatic uninvolved, but not normal, stem keratinocytes. , 1995, The Journal of clinical investigation.
[111] H. E. Hansen,et al. Psoriasis in monozygotic twins: variations in expression in individuals with identical genetic constitution. , 1982, Acta dermato-venereologica.