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Site‐specific immunophenotyping of keloid disease demonstrates immune upregulation and the presence of lymphoid aggregates
Author(s) -
Bagabir R.,
Byers R.J.,
Chaudhry I.H.,
Müller W.,
Paus R.,
Bayat A.
Publication year - 2012
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2012.11190.x
Subject(s) - keloid , pathology , immunophenotyping , inflammation , immune system , medicine , immunohistochemistry , pathogenesis , immunology , antigen
Summary Background Keloid disease (KD) is a common fibroproliferative disorder of unknown aetiology. T cells and macrophages are increased in KD and are thought to contribute to its pathogenesis. However, while a link between inflammation and fibrotic disorders is well known for other disorders, it remains undetermined in KD. Objectives Systematically to immunophenotype the inflammatory infiltrate of KD in situ in a site‐specific manner, and to compare this with normal skin and scar tissue. Methods Sixty‐eight keloid cases were screened for the presence of all three (intralesional, perilesional and extralesional) keloid‐associated specific tissue sites. Subsequently, a complete set of 25 keloid biopsies (from different patients) was compared with normal skin ( n = 11) and normal scar ( n = 11) samples and subjected to systematic, site‐specific quantitative immunohistomorphometry and histochemistry, using a range of immunological markers of B cells, T cells, macrophages, mast cells (MCs) and Langerhans cells. Results T cells, B cells, degranulated and mature MCs (coexpressing OX40 ligand) and alternative macrophages (M2) were all significantly increased in intralesional and perilesional KD sites compared with normal skin and scar tissue ( P < 0·05). Additionally, 10 of 68 KD cases (15%) showed the presence of distinctive lymphoid aggregates, which resembled mucosa‐associated lymphoid tissue (MALT). Conclusions The increased number and activity of MCs and M2 may implicate inflammation in the fibrotic process in KD. The distinct KD‐associated lymphoid aggregate resembles MALT, for which we propose the term ‘keloid‐associated lymphoid tissue’ (KALT). It may perpetuate inflammatory stimuli that promote KD growth. KALT, MCs and M2 are promising novel targets for future KD therapy.