ArticleJournal of clinical pathology2007
Immunohistological analysis of immune cells in blistering skin lesions.
Article in Journal of clinical pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- The emerging role of T cells in pemphigus vulgaris: a systematic review.Clinical and experimental medicine · 2023Pooled it
- Infected wound repair correlates with collagen I induction and NOX2 activation by cold atmospheric plasma.NPJ Regenerative medicine · 2024Article
- Lymphocytic infiltration as a marker of disease severity in patients with bullous pemphigoid-A case series.Clinical case reports · 2024Article
- Granzyme B in Autoimmune Skin Disease.Biomolecules · 2023Review
- Therapeutic effects of Fc gamma RIV inhibition are mediated by selectively blocking immune complex-induced neutrophil activation in epidermolysis bullosa acquisita.Frontiers in immunology · 2022Article
- Granzyme B inhibition reduces disease severity in autoimmune blistering diseases.Nature communications · 2021Article
- Proteases in Pemphigoid Diseases.Frontiers in immunology · 2019Review
- Unraveling the ECM-Immune Cell Crosstalk in Skin Diseases.Frontiers in cell and developmental biology · 2019Review
- Granzyme B is elevated in autoimmune blistering diseases and cleaves key anchoring proteins of the dermal-epidermal junction.Scientific reports · 2018Article
- Epidermolysis Bullosa Acquisita: The 2019 Update.Frontiers in medicine · 2018Review
- Histologic characterization of cellular infiltration in autoimmune subepidermal bullous diseases in a tertiary hospital in Saudi Arabia.Clinical, cosmetic and investigational dermatology · 2018Article
- Correlation between IL36α and IL17 and Activity of the Disease in Selected Autoimmune Blistering Diseases.Mediators of inflammation · 2017Article
- Intracellular versus extracellular granzyme B in immunity and disease: challenging the dogma.Laboratory investigation; a journal of technical methods and pathology · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBullous skin lesions are characterised by the presence of intraepidermal or subepidermal bullae. Although inflammatory cell infiltrate is a constant feature in these lesions, their immunophenotypic characterisation is still incomplete.
aimTo determine whether the development of bullous skin diseases is associated with changes in the inflammatory cell infiltrate. MATERIALS AND
methods34 cases representing lesions with both intraepidermal and subepidermal bullae were examined using immunoperoxidase staining methods and antibodies targeting antigens for histiocytes (CD68), B cells (CD20+), T cells (CD3+), T cells with cytotoxic potential (T cell intracellular associated antigen, TIA1+) and activity (granzyme B, GRB+). The adjacent normal skin (lesions) and an additional five cases of normal skin were also examined (controls).
resultsThe transition from normal skin to lesional skin (lesions with intraepidermal and subepidermal bullae) was associated with a significant increase (p< or =0.05) in the density of total inflammatory cell infiltrate, CD68+ cells, CD3+ T lymphocytes, CD20+ B lymphocytes, TIA1+ -resting cytotoxic T cells and GRB+ T cells with cytotoxic activity.
conclusionsThe increase in inflammatory cell infiltrate during the transition from normal to lesional skin may reflect the presence of an increased antigenicity of the lesional cells or a response to some basement membrane components. CD68+ and CD3+ cells, especially the resting cytotoxic ones, achieved numerical dominance in these lesions. Cell-mediated immunity seems to have critical role in the development of these lesions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.