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Lesional Skin Biopsies (lesional + skin_biopsy)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Effect of PUVA, narrow-band UVB and cyclosporin on inflammatory cells of the psoriatic plaque

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 3 2007
Gul Erkin
Background:, Because antigen presenting is necessary for T-cell activation, antigen-presenting cells should be involved in the pathogenesis of psoriasis. In this study, our purpose was to evaluate and compare effects of PUVA, cyclosporine A and narrow-band UVB on dendritic cells and activated lymphocytes in the psoriatic lesions. Methods:, Forty-five volunteered patients (15 patients in each treatment group as PUVA, cyclosporin A and narrow-band UVB) were enrolled in this study. Lesional skin biopsies were taken from each patient before and after treatments. Fresh frozen biopsies were studied for the expressions of CD1a, CD68, CD86, CD4, CD8 and HLA-DR proteins by immunohistochemistry. Results:, There was no correlation between severity of the lesions and expressions of the antigens. Only PUVA significantly decreased CD1a+ epidermal Langerhans cells' (LCs) counts. Treatment modalities decreased expression of costimulator CD86, and most of them decrease antigen-presenting capacity of skin by decreasing HLA class-II expression. Conclusions:, All treatment modalities equally reduce lymphocytes, macrophages and dendritic cells. PUVA is the only treatment that decreases epidermal LCs. All treatments effectively diminish expression of CD86 and inhibit this step of inflammation. [source]

The expression pattern of interferon-inducible proteins reflects the characteristic histological distribution of infiltrating immune cells in different cutaneous lupus erythematosus subsets

BRITISH JOURNAL OF DERMATOLOGY, Issue 4 2007
J. Wenzel
Summary Background, Plasmacytoid dendritic cells and type I interferons (IFNs) are supposed to play a central proinflammatory role in the pathogenesis of cutaneous lupus erythematosus (LE). The IFN-inducible chemokines CXCL9 and CXCL10 are involved in recruiting CXCR3+ effector lymphocytes from the peripheral blood into skin lesions of LE. We hypothesized that the expression pattern of IFN-inducible proteins reflects the characteristic distribution of the inflammatory infiltrate in different subsets of cutaneous LE. Objectives, To test this hypothesis in patients with LE. Methods, Lesional skin biopsies taken from patients with different subsets of LE [chronic discoid LE (CDLE), n = 12; subacute cutaneous LE (SCLE), n = 5; LE tumidus (LET), n = 4; LE profundus (LEP), n = 6] were investigated by immunohistochemistry using monoclonal antibodies to the lymphocyte surface markers CD3, CD4, CD8, CD20 and CD68, the cytotoxic proteins Tia1 and granzyme B, the chemokine receptor CXCR3, the specifically type I IFN-inducible protein myxovirus protein A (MxA) and the chemokines CXCL9 and CXCL10. Results, The expression pattern of MxA followed the distribution of the inflammatory infiltrate typically seen in the investigated cutaneous LE subsets. In CDLE and SCLE, expression was focused in the epidermis and upper dermis, while in LET a perivascular and in LEP a subcutaneous pattern was found. Similar findings were obtained for CXCL9 and CXCL10. Conclusions, Our results demonstrate a close morphological association between the expression pattern of IFN-inducible proteins and the distribution of CXCR3+ CD3+ lymphocytes in all investigated subsets of cutaneous LE. This supports the importance of an IFN-driven inflammation in this condition. Infiltrating lymphocytes carrying CXCL10 in their granules might amplify the lesional inflammation and be responsible for the chronic course of this disease. [source]

Examination of mycosis fungoides for the presence of Epstein,Barr virus and human herpesvirus-6 by polymerase chain reaction

JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 5 2001
E Erkek
Abstract Background The aetiology of cutaneous T-cell lymphoma (CTCL) remains unknown despite numerous investigations. In recent years, retroviruses and human herpesviruses have been implicated to play a causal part in CTCL. Objective The aim of this study was to elucidate the possible aetiopathogenetic role of human herpesviruses (HHV) in mycosis fungoides (MF). Methods Polymerase chain reaction was used to study formalin-fixed, paraffin-embedded lesional skin biopsies from 92 subjects with MF to evidence possible presence of Epstein,Barr virus (EBV) and HHV-6. Results Biopsy specimens from nine subjects (9.8%) evidenced EBV DNA, whereas all except one of the subjects (1.1%) lacked HHV-6 DNA. Conclusions Although these findings do not support a primary aetiological role for EBV and HHV-6 in classical CTCL, the possibility remains that both viruses, particularly EBV, may act as potential cofactors in the development of CTCL. [source]

Up-regulation of CCL17, CCL22 and CCR4 in drug-induced maculopapular exanthema

CLINICAL & EXPERIMENTAL ALLERGY, Issue 5 2007
B. Tapia
Summary Background Maculopapular exanthema has been reported to be the most frequently drug-induced cutaneous reaction. Although T lymphocytes are involved in the pathomechanism of this disease, little is know about the recruitment of these cells to the skin. Objective The aim of this work is to study the role of the chemokines TARC/CCL17 and MDC/CCL22 in the lymphocyte trafficking to affected skin in drug-induced exanthemas. Methods Real-time PCR was performed to quantify gene expression levels of CCL17, CCL22 and their receptor CCR4 in lesional skin biopsies and in peripheral blood mononuclear cells from patients. CCL27 and CCL22 proteins were detected in the skin by immunochemistry. Protein expression of CCR4 was determined by flow cytometry in peripheral blood lymphocytes. Functional migration assays to CCL17 and CCL22 were assessed to compare the migratory responses of peripheral blood lymphocytes from patients and healthy subjects. Results CCL17 and CCL22 were up-regulated in maculopapular exanthema-affected skin. CCR4 mRNA levels and protein expression were increased in peripheral blood mononuclear cells during the acute phase of the disease. The increased expression of the receptor was consistent with a higher response of peripheral blood lymphocytes to CCL17 and CCL22 compared with the migratory response in healthy donors. Conclusion TARC/CCL17 and MDC/CCL22 might cooperate in attracting T lymphocytes to skin in drug-induced maculopapular exanthemas. [source]