Literature DB >> 10648117

CD69, HLA-DR and the IL-2R identify persistently activated T cells in psoriasis vulgaris lesional skin: blood and skin comparisons by flow cytometry.

K Ferenczi1, L Burack, M Pope, J G Krueger, L M Austin.   

Abstract

Many lymphocyte-activation-associated molecules are observed by immunohistochemistry in psoriasis vulgaris lesional skin. Non-T cells in lesional skin also express these molecules. We quantitatively measured the number of T cells expressing cell surface activation-associated molecules (CD69, CD25, CD122, HLA-DR) and co-stimulatory molecules (CD28, CTLA-4, CD80, CD86), including a Type 2 T cell marker (CD30) and CD11b, by flow cytometry of skin and peripheral blood. T cells in single cell suspensions of psoriatic lesional-epidermis-expressed HLA-DR (86%), CD69 (59%), CD25 (55%), CD122 (44%), and CD28 (91%). Dermal T cells showed similar percentages except for CD69 (17%). CD69 was found directly in lesional skin biopsies by immunohistochemistry. Both CD4 and CD8 subsets from lesional skin contained large populations of CD25+ cells with a bias towards CD8 activation in the epidermis and towards CD4 activation in the dermis. CD86, CD80, CTLA-4, CD30 and CD11b were expressed by less than 23% of the T cell populations from both the epidermis and dermis. CD30+CD4+ cells were found two-fold over CD8+ T cells. These results show that the majority of lesional lymphocytes are persistently activated. We also found the majority of Type 2 associated markers primarily on the CD4+ epidermal T cell population. Psoriatic blood contained elevated levels of T cells expressing CD25, primarily within the CD8+ subset. Thus the majority of lesional T cells expressed the three primary activation markers, while psoriatic blood T cells were distinguished by an increase in CD25, specifically within the CTL population. Copyright 2000 Academic Press.

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Year:  2000        PMID: 10648117     DOI: 10.1006/jaut.1999.0343

Source DB:  PubMed          Journal:  J Autoimmun        ISSN: 0896-8411            Impact factor:   7.094


  34 in total

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2.  Dysfunctional blood and target tissue CD4+CD25high regulatory T cells in psoriasis: mechanism underlying unrestrained pathogenic effector T cell proliferation.

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Review 3.  Immunopathogenesis of psoriasis.

Authors:  Brian J Nickoloff; Jian-Zhong Qin; Frank O Nestle
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Journal:  J Invest Dermatol       Date:  2014-02-25       Impact factor: 8.551

5.  Myeloid-Derived Suppressor Cells in Psoriasis Are an Expanded Population Exhibiting Diverse T-Cell-Suppressor Mechanisms.

Authors:  Lauren Y Cao; Jin-Sung Chung; Takahiro Teshima; Lawrence Feigenbaum; Ponciano D Cruz; Heidi T Jacobe; Benjamin F Chong; Kiyoshi Ariizumi
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6.  Mast cell CD30 ligand is upregulated in cutaneous inflammation and mediates degranulation-independent chemokine secretion.

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Authors:  Adil I Daud; Kimberly Loo; Mariela L Pauli; Robert Sanchez-Rodriguez; Priscila Munoz Sandoval; Keyon Taravati; Katy Tsai; Adi Nosrati; Lorenzo Nardo; Michael D Alvarado; Alain P Algazi; Miguel H Pampaloni; Iryna V Lobach; Jimmy Hwang; Robert H Pierce; Iris K Gratz; Matthew F Krummel; Michael D Rosenblum
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Review 8.  The Potential Role of Inhibitory Receptors in the Treatment of Psoriasis.

Authors:  Neha Shah; Sabina Sandigursky; Adam Mor
Journal:  Bull Hosp Jt Dis (2013)       Date:  2017-05

9.  Role of a histamine 4 receptor as an anti-inflammatory target in carrageenan-induced pleurisy in mice.

Authors:  Sheikh Fayaz Ahmad; Khairy M A Zoheir; Hala E Abdel-Hamied; Ibrahim Alrashidi; Sabry M Attia; Saleh A Bakheet; Abdelkader E Ashour; Adel R A Abd-Allah
Journal:  Immunology       Date:  2014-07       Impact factor: 7.397

Review 10.  Immunology of psoriasis.

Authors:  Michelle A Lowes; Mayte Suárez-Fariñas; James G Krueger
Journal:  Annu Rev Immunol       Date:  2014       Impact factor: 28.527

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