The role of T lymphocytes and cytokines in the pathogenesis of pemphigoid gestationis

Fabbri, Paolo; Caproni, Marzia; Berti, Samantha; Bianchi, Beatrice; Amato, L.; Pità, Ornella De; Frezzolini, Alessandra

doi:10.1046/j.1365-2133.2003.05265.x

Cited by 30 publications

(19 citation statements)

References 32 publications

(63 reference statements)

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“…4 5 16 Our finding of increased inflammatory cell infiltrate in the bullous skin lesions is consistent with results from previous studies. [17][18][19] This infiltrate consisted of an admixture of both acute (neutrophils, eosinophils and lymphocytes) and chronic (lymphocytes, histiocytes and plasma cells) inflammatory cells, with the acute cells being the predominant cell populations. In some lesions (pustular psoriasis, familial cutaneous peeling, chronic contact dermatitis and lichen planus atrophicus), this admixture of cells showed sharp peaking of one of the inflammatory cell components (neutrophils for pustular psoriasis and lymphocytes for the others).…”

Section: Discussionmentioning

confidence: 99%

Immunohistological analysis of immune cells in blistering skin lesions

Hussein

Ali²,

Omar³

2007

J Clin Pathol

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Background: Bullous 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. Aim: To determine whether the development of bullous skin diseases is associated with changes in the inflammatory cell infiltrate. Materials and methods: 34 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). Results: The transition from normal skin to lesional skin (lesions with intraepidermal and subepidermal bullae) was associated with a significant increase (p(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. Conclusions: The 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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Section: Discussionmentioning

confidence: 99%

Immunohistological analysis of immune cells in blistering skin lesions

Hussein

Ali²,

Omar³

2007

J Clin Pathol

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“…For example, in the autoimmune blistering disorders, bullous pemphigoid, herpes gestationis and pemphigus vulgaris there is a clear Th2 response which is observed early in the disease, but it is unclear whether it comes before the full thickness epithelial disruption or as a consequence of it (Arbesman et al , 1974; Borrego et al , 1999; Bushkell and Jordon, 1983; De Pita et al , 1997; Fabbri et al , 2003; Feliciani et al , 1999; Nagel et al , 2010) (Table 1). Similarly, in the genodermatosis, epidermolysis bullosa pruriginosa (OMIM 60412) (Mellerio et al , 1999; Yamasaki et al , 1997), a skin fragility disorder caused by mutations in the COL7A1 gene, and characterized by anchoring fibril abnormalities and sublamina densa blistering, the patients have been reported to have high serum IgE and eosinophilia (McGrath et al , 1994) (Table 1).…”

Section: Skin Barrier Defects Promote Allergen Sensitization - Evmentioning

confidence: 99%

Skin Barrier Disruption: A Requirement for Allergen Sensitization?

Benedetto

Kubo

Beck

2012

Journal of Investigative Dermatology

277

252

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For at least half a century, noninvasive techniques have been available to quantify skin barrier function, and these have shown that a number of human skin conditions and disorders are associated with defects in skin permeability. In the last decade, several genes responsible for skin barrier defects observed in both monogenetic and complex, polygenic disorders have been elucidated and functionally characterized. This has led to an explosion of work in the last six years that has identified pathways connecting epidermal barrier disruption and antigen uptake as well as the quality and/or magnitude of the antigen-specific adaptive immune response. This review will introduce the notion that diseases arise from the dynamic crosstalk that occurs between the skin barrier and immune system using atopic dermatitis or eczema as the disease prototype. Nevertheless, the concepts put forth are highly relevant to a number of antigen-driven disorders for which skin barrier is at least transiently compromised such as psoriasis, allergic contact dermatitis and blistering disorders.

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“…It is considered that HLA mismatch between mother and fetus triggers an immune response which initiates an allogenic response to placental BMZ, which then cross reacts with skin. Recent immunohistochemical studies have identified a T-cell population with a prevalent T helper (Th2) phenotype in the lesional skin of PG subjects,[4] which may be implicated in the recognition of self-antigens and production of pathogenic autoantibodies.…”

Section: Discussionmentioning

confidence: 99%

Postpartum pemphigoid gestationis

et al. 2012

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Pemphigoid gestationis (PG) or herpes gestationis is a rare autoimmune subepidermal blistering disorder associated with pregnancy. The condition typically develops during the second or third trimester of pregnancy, but has been rarely reported in the first trimester and postpartum period. Here, we report a case of PG that presented for the first time in the postpartum period, associated with a low birth weight baby.

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The role of T lymphocytes and cytokines in the pathogenesis of pemphigoid gestationis

Abstract: These data suggest that an inflammatory infiltrate is involved in the production of PG bullous lesions. In particular, we assume that the Th2 cells might be implicated in the very early stages of autoimmune response and may exercise a broad influence in blister formation in this disease.

Cited by 30 publications

References 32 publications

Immunohistological analysis of immune cells in blistering skin lesions

Immunohistological analysis of immune cells in blistering skin lesions

Skin Barrier Disruption: A Requirement for Allergen Sensitization?

Postpartum pemphigoid gestationis

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