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“Up-regulation of Id1 in peripheral blood of psoriatic patients”, vol. 9, pp. 2239-2247, 2010.
, Abrams JR, Kelley SL, Hayes E, Kikuchi T, et al. (2000). Blockade of T lymphocyte costimulation with cytotoxic T lymphocyte-associated antigen 4-immunoglobulin (CTLA4Ig) reverses the cellular pathology of psoriatic plaques, including the activation of keratinocytes, dendritic cells, and endothelial cells. J. Exp. Med. 192: 681-694.
http://dx.doi.org/10.1084/jem.192.5.681
PMid:10974034 PMCid:2193278
Ackerman AB (1978). Psoriasis. In: Histologic Diagnosis of Inflammatory Skin Diseases (Ackerman AB, ed.). Lea and Febiger, Philadelphia, 251-256.
Austin LM, Ozawa M, Kikuchi T, Walters IB, et al. (1999). The majority of epidermal T cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-gamma, interleukin-2, and tumor necrosis factor-alpha, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations: a type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients. J. Invest. Dermatol. 113: 752-759.
http://dx.doi.org/10.1046/j.1523-1747.1999.00749.x
PMid:10571730
Bata-Csorgo Z, Hammerberg C, Voorhees JJ and Cooper KD (1995a). Intralesional T-lymphocyte activation as a mediator of psoriatic epidermal hyperplasia. J. Invest. Dermatol. 105: 89S-94S.
http://dx.doi.org/10.1038/jid.1995.18
PMid:7616005
Bata-Csorgo Z, Hammerberg C, Voorhees JJ and Cooper KD (1995b). 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. J. Clin. Invest. 95: 317-327.
http://dx.doi.org/10.1172/JCI117659
PMid:7529261 PMCid:295434
Bjorntorp E, Parsa R, Thornemo M, Wennberg AM, et al. (2003). The helix-loop-helix transcription factor Id1 is highly expressed in psoriatic involved skin. Acta Derm. Venereol. 83: 403-409.
http://dx.doi.org/10.1080/00015550310015806
PMid:14690332
Böhm I (2006). Quantification of absolute peripheral white blood cells and their subsets in patients with lupus erythematosus: comparison with other inflammatory diseases with and without autoimmune background. Biomed. Pharmacother. 60: 92-95.
http://dx.doi.org/10.1016/j.biopha.2005.06.007
PMid:16256301
Bonifati C, Carducci M, Cordiali FP, Trento E, et al. (1994). Correlated increases of tumour necrosis factor-alpha, interleukin-6 and granulocyte monocyte-colony stimulating factor levels in suction blister fluids and sera of psoriatic patients - relationships with disease severity. Clin. Exp. Dermatol. 19: 383-387.
http://dx.doi.org/10.1111/j.1365-2230.1994.tb02687.x
PMid:7955493
Ettehadi P, Greaves MW, Wallach D, Aderka D, et al. (1994). Elevated tumour necrosis factor-alpha (TNF-alpha) biological activity in psoriatic skin lesions. Clin. Exp. Immunol. 96: 146-151.
http://dx.doi.org/10.1111/j.1365-2249.1994.tb06244.x
PMid:8149659 PMCid:1534536
Friedrich M, Krammig S, Henze M, Docke WD, et al. (2000). Flow cytometric characterization of lesional T cells in psoriasis: intracellular cytokine and surface antigen expression indicates an activated, memory/effector type 1 immunophenotype. Arch. Dermatol. Res. 292: 519-521.
http://dx.doi.org/10.1007/s004030000167
PMid:11142774
Gottlieb AB, Lebwohl M, Shirin S, Sherr A, et al. (2000). Anti-CD4 monoclonal antibody treatment of moderate to severe psoriasis vulgaris: results of a pilot, multicenter, multiple-dose, placebo-controlled study. J. Am. Acad. Dermatol. 43: 595-604.
http://dx.doi.org/10.1067/mjd.2000.107945
PMid:11004613
Gottlieb AB, Masud S, Ramamurthi R, Abdulghani A, et al. (2003). Pharmacodynamic and pharmacokinetic response to anti-tumor necrosis factor-alpha monoclonal antibody (infliximab) treatment of moderate to severe psoriasis vulgaris. J. Am. Acad. Dermatol. 48: 68-75.
http://dx.doi.org/10.1067/mjd.2003.10
PMid:12522373
Gottlieb SL, Gilleaudeau P, Johnson R, Estes L, et al. (1995). Response of psoriasis to a lymphocyte-selective toxin (DAB389IL-2) suggests a primary immune, but not keratinocyte, pathogenic basis. Nat. Med. 1: 442-447.
http://dx.doi.org/10.1038/nm0595-442
PMid:7585092
Henseler T (1998). Genetics of psoriasis. Arch. Dermatol. Res. 290: 463-476.
http://dx.doi.org/10.1007/s004030050338
PMid:9808339
Hu LH, Chen FH, Li YR and Wang L (2004). Real-time determination of human telomerase reverse transcriptase mRNA in gastric cancer. World J. Gastroenterol. 10: 3514-3517.
PMid:15526376
Ishiguro A, Spirin KS, Shiohara M, Tobler A, et al. (1996). Id2 expression increases with differentiation of human myeloid cells. Blood 87: 5225-5231.
PMid:8652837
Jeffes EW III, McCullough JL, Pittelkow MR, McCormick A, et al. (1995). Methotrexate therapy of psoriasis: differential sensitivity of proliferating lymphoid and epithelial cells to the cytotoxic and growth-inhibitory effects of methotrexate. J. Invest. Dermatol. 104: 183-188.
http://dx.doi.org/10.1111/1523-1747.ep12612745
PMid:7829873
Ketboonlue K (2007). Detection of Serotonin and Development of Laboratory Technique for Detecting Autoantibodies to Serotonin in the Psoriatic Patients' Blood. Master's thesis, Chulalongkorn University, Bangkok.
Krueger JG, Walters IB, Miyazawa M, Gilleaudeau P, et al. (2000). Successful in vivo blockade of CD25 (high-affinity interleukin 2 receptor) on T cells by administration of humanized anti-Tac antibody to patients with psoriasis. J. Am. Acad. Dermatol. 43: 448-458.
http://dx.doi.org/10.1067/mjd.2000.106515
PMid:10954656
Kupper TS (2003). Immunologic targets in psoriasis. N. Engl. J. Med. 349: 1987-1990.
http://dx.doi.org/10.1056/NEJMp038164
PMid:14627782
Lowes MA, Bowcock AM and Krueger JG (2007). Pathogenesis and therapy of psoriasis. Nature 445: 866-873.
http://dx.doi.org/10.1038/nature05663
PMid:17314973
Mark EB, Jonsson M, Asp J, Wennberg AM, et al. (2006). Expression of genes involved in the regulation of p16 in psoriatic involved skin. Arch. Dermatol. Res. 297: 459-467.
http://dx.doi.org/10.1007/s00403-006-0649-1
PMid:16552541
Marsland AM and Griffiths CE (2002). The macrolide immunosuppressants in dermatology: mechanisms of action. Eur. J. Dermatol. 12: 618-622.
PMid:12459545
Nair RP, Duffin KC, Helms C, Ding J, et al. (2009). Genome-wide scan reveals association of psoriasis with IL-23 and NF-kappaB pathways. Nat. Genet. 41: 199-204.
http://dx.doi.org/10.1038/ng.311
PMid:19169254 PMCid:2745122
Naldi L (2010). Scoring and monitoring the severity of psoriasis. What is the preferred method? What is the ideal method? Is PASI passe? Facts and controversies. Clin. Dermatol. 28: 67-72.
http://dx.doi.org/10.1016/j.clindermatol.2009.03.001
PMid:20082954
Ockenfels HM, Nussbaum G, Schultewolter T, Mertins K, et al. (1995). Tyrosine phosphorylation in psoriatic T cells is modulated by drugs that induce or improve psoriasis. Dermatology 191: 217-225.
http://dx.doi.org/10.1159/000246549
PMid:8534940
Ozawa A, Sugai J, Ohkido M, Ohtsuki M, et al. (1999). Cyclosporin in psoriasis: continuous monotherapy versus intermittent long-term therapy. Eur. J. Dermatol. 9: 218-223.
PMid:10210789
Prinz JC, Gross B, Vollmer S, Trommler P, et al. (1994). T cell clones from psoriasis skin lesions can promote keratinocyte proliferation in vitro via secreted products. Eur. J. Immunol. 24: 593-598.
http://dx.doi.org/10.1002/eji.1830240315
PMid:8125129
Rivera R and Murre C (2001). The regulation and function of the Id proteins in lymphocyte development. Oncogene 20: 8308-8316.
http://dx.doi.org/10.1038/sj.onc.1205091
PMid:11840323
Rocha-Pereira P, Santos-Silva A, Rebelo I, Figneiredo A, et al. (2004). Erythrocyte damage in mild and severe psoriasis. Br. J. Dermatol. 150: 232-244.
http://dx.doi.org/10.1111/j.1365-2133.2004.05801.x
PMid:14996093
Ronpirin C and Tencomnao T (2010). Psoriasis: A review of the role of serotonergic system. Afr. J. Biotechnol. 9: 1528- 1534.
Sakurai D, Yamaguchi A, Tsuchiya N, Yamamoto K, et al. (2001). Expression of ID family genes in the synovia from patients with rheumatoid arthritis. Biochem. Biophys. Res. Commun. 284: 436-442.
http://dx.doi.org/10.1006/bbrc.2001.4974
PMid:11394898
Schön MP and Boehncke WH (2005). Psoriasis. N. Engl. J. Med. 352: 1899-1912.
http://dx.doi.org/10.1056/NEJMra041320
PMid:15872205
Suh HC, Leeanansaksiri W, Ji M, Klarmann KD, et al. (2008). Id1 immortalizes hematopoietic progenitors in vitro and promotes a myeloproliferative disease in vivo. Oncogene 27: 5612-5623.
http://dx.doi.org/10.1038/onc.2008.175
PMid:18542061 PMCid:3073486
Szabo SK, Hammerberg C, Yoshida Y, Bata-Csorgo Z, et al. (1998). Identification and quantitation of interferon-gamma producing T cells in psoriatic lesions: localization to both CD4+ and CD8+ subsets. J. Invest. Dermatol. 111: 1072- 1078.
http://dx.doi.org/10.1046/j.1523-1747.1998.00419.x
PMid:9856819
Tam WF, Gu TL, Chen J, Lee BH, et al. (2008). Id1 is a common downstream target of oncogenic tyrosine kinases in leukemic cells. Blood 112: 1981-1992.
http://dx.doi.org/10.1182/blood-2007-07-103010
PMid:18559972 PMCid:2518899
Vallat VP, Gilleaudeau P, Battat L, Wolfe J, et al. (1994). PUVA bath therapy strongly suppresses immunological and epidermal activation in psoriasis: a possible cellular basis for remittive therapy. J. Exp. Med. 180: 283-296.
http://dx.doi.org/10.1084/jem.180.1.283
PMid:7516410
Vollmer S, Menssen A, Trommler P, Schendel D, et al. (1994). T lymphocytes derived from skin lesions of patients with psoriasis vulgaris express a novel cytokine pattern that is distinct from that of T helper type 1 and T helper type 2 cells. Eur. J. Immunol. 24: 2377-2382.
http://dx.doi.org/10.1002/eji.1830241018
PMid:7925564
Wong YC, Wang X and Ling MT (2004). Id-1 expression and cell survival. Apoptosis 9: 279-289.
http://dx.doi.org/10.1023/B:APPT.0000025804.25396.79
PMid:15258459
Yang Y, Liou HC and Sun XH (2006). Id1 potentiates NF-kappaB activation upon T cell receptor signaling. J. Biol. Chem. 281: 34989-34996.
http://dx.doi.org/10.1074/jbc.M608078200
PMid:17012234