Identification of a Th2‐ and Th17‐skewed immune phenotype in chronic urticaria with Th22 reduction dependent on autoimmunity and thyroid disease markers

Journal of Cutaneous Pathology - Tập 43 Số 4 - Trang 372-378 - 2016
Andrea P. Moy1, Mandakolathur R. Murali2,1, Rosalynn M. Nazarian1,3,4,5
1Pathology Service, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
2Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
3Pathology Service, Massachusetts General Hospital, 55 Fruit Street, Warren 829A, Boston, MA 02114, USA
4Rosalynn M. Nazarian, MD,
5Tel: (617) 726 8304

Tóm tắt

AbstractBackgroundChronic urticaria is a condition with many inciting factors and often presents a therapeutic challenge to clinicians. In addition to a central role for mast cells, an immune dysregulated state related to cytokine/chemokine alterations is increasingly being recognized.MethodsBiopsies of chronic urticaria (n = 11) and normal skin (n = 5) were evaluated with immunostains for CD117, CD3 and dual stains for CD4/T‐bet, GATA‐3, STAT‐3 or BNC‐2 (transcription factors specific and mutually exclusive for Th1, Th2, Th17 and Th22 cells, respectively). Clinical data, including autoantibodies and thyroid function tests, and the number of CD117+ mast cells and percent of Th1, Th2, Th17 and Th22 of CD3+ T‐cells were compared.ResultsTh2 cells and Th17 cells were significantly more frequent in chronic urticaria than controls. In contrast, there was no significant difference in mast cells, Th1 cells or Th22 cells. Three of nine chronic urticaria patients had evidence of autoimmune disease; biopsies from these patients trended toward a greater number of mast cells and decreased percent of Th‐cell subtypes as compared with those without autoimmunity markers, with significantly less Th22 cells.ConclusionsThese findings provide novel insight into the role of Th2 and Th17 in chronic urticaria pathophysiology and may impact therapy.

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Tài liệu tham khảo

10.1155/2014/674709

10.1016/j.jaip.2014.04.011

10.1016/j.anai.2014.02.014

10.1056/NEJMoa1215372

10.1038/jid.2014.306

10.1016/0091-6749(89)90180-2

10.1067/mai.2003.1605

10.1111/j.1365-2133.2005.06646.x

10.1111/ddg.12194

10.1067/mai.2002.123236

10.1034/j.1600-065X.2001.790109.x

10.1186/1476-7961-8-3

10.1038/jid.2010.175

10.1159/000345401

10.1111/jdv.12124

10.1016/j.jaut.2015.04.006

10.1016/j.jdermsci.2013.04.028

10.1001/jamadermatol.2015.2

10.1111/all.12313

10.1001/archdermatol.2007.5

10.1016/0091-6749(78)90113-6

10.1016/0091-6749(86)90240-X

10.1016/S0091-6749(95)70055-2

10.1034/j.1398-9995.2001.00296.x

Caproni M, 2005, Chronic urticaria: infiltrating cells and related cytokines in autologous serum‐induced wheals, J Allergy Clin Immunol, 114, 284

10.1046/j.1365-2133.1999.02815.x

10.1016/j.iac.2004.01.003

10.1016/S0091-6749(99)70129-6

10.1016/S0091-6749(99)70475-6

10.1172/JCI511

10.1111/j.1365-2222.2006.02494.x

10.1016/j.jaci.2007.05.008

10.1038/jid.2008.416

10.1016/j.anai.2012.10.020

10.1385/CRIAI:23:2:195

10.1034/j.1600-0625.2003.00010.x

10.1159/000066772

10.1111/bjd.13621

10.1097/ACI.0000000000000133

10.1067/mai.2003.1414

10.1111/j.1365-2133.2008.08902.x

10.1038/jid.2008.111

10.1038/jid.2009.399

Eyerich S, 2009, Th22 cells represent a distinct human T cell subset involved in epidermal immunity and remodeling, J Clin Invest, 119, 3573

10.1056/NEJMra0707449

10.1038/nri3536

10.1111/j.1600-6143.2006.01704.x

10.1155/2011/259867

10.1111/cup.12471

10.1016/S0190-9622(99)70495-0

10.1016/j.jaci.2013.01.029

10.1016/j.bbadis.2011.02.009

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Journal of Cutaneous Pathology

Tập 43 Số 4

372-378

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