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Lymphocytic Inflammation (lymphocytic + inflammation)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Enhanced type I interferon signaling and recruitment of chemokine receptor CXCR3-expressing lymphocytes into the skin following treatment with the TLR7-agonist imiquimod

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 4 2005
Joerg Wenzel
Introduction:, Imiquimod (AldaraÔ) is an immune response modifier approved for the topical treatment of external genital and perianal warts which can mediate regression of several cutaneous malignancies [basal cell carcinoma (BCC), Bowen's disease, actinic keratosis, and metastasis of malignant melanoma]. Recently, it was discovered that imiquimod acts through the toll-like receptor (TLR) 7. We hypothesize that TLR7-signaling strongly induces the production of interferon (IFN) ,, which is able to enhance Th1-mediated cellular antiviral and antitumor immunity. Patients and methods:, In the present study we analyzed the expression of MxA, a protein specifically induced by type I IFNs during topical imiquimod treatment in several patients suffering from different cutaneous malignancies (BCC, cutaneous metastasis of melanoma, and breast cancer), and characterized the inflammatory infiltrate, along with the expression of chemokine receptor CXCR3, by immunohistochemistry. Results:, Treatment with the TLR7-agonist imiquimod induced a significant lesional lymphocytic inflammation, associated with strong expression of MxA, indicating the induction of type I IFN signaling. The extent of lesional MxA staining closely correlated with the number of infiltrating T lymphocytes and the expression of the chemokine receptor CXCR3, characteristic for Th1-biased immune responses. Discussion:, Our in vivo results suggest an important role for TLR7-induced production of type I IFN, which links innate and adaptive immunity and promotes specific Th1-biased cellular immune response capable of eliminating cutaneous malignancies. MxA appears to be a valuable parameter to demonstrate IFN-type I expression in imiquimod therapy. [source]

Mid-dermal elastolysis preceded by acute neutrophilic dermatosis

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2004
Kevan G. Lewis
Background:, Mid-dermal elastolysis is a rare idiopathic elastic tissue disorder that is characterized by localized patches of finely wrinkled skin and a ,band-like' loss of elastic tissue in the mid-reticular dermis. Lesions may be preceded by erythema and/or urticaria, and histological examination of inflamed lesional skin may demonstrate lymphohistiocytic dermal infiltration. Case report:, We report a case of mid-dermal elastolysis in a 31-year-old woman who developed multiple erythematous and urticarial plaques on the arms and trunk. Histologic examination of a representative lesion revealed a neutrophilic infiltrate and a normal pattern of elastic tissue. Several months later, the erythema and urticaria was noted to have resolved, leaving soft, pendulous plaques with overlying finely wrinkled skin. A follow-up biopsy at this time showed minimal lymphocytic inflammation but almost complete absence of elastic tissue in the mid-reticular dermis. Conclusions:, To our knowledge, acute neutrophilic dermatosis resulting in mid-dermal elastolysis has not been previously described. This observation lends support to an emerging theory that the pathogenesis of mid-dermal elastolysis may be inflammatory. [source]

Increased metal allergy in patients with failed metal-on-metal hip arthroplasty and peri-implant T-lymphocytic inflammation

ALLERGY, Issue 8 2009
P. Thomas
Background:, In 16 patients with revised metal-on-metal arthroplasty and peri-implant lymphocytic inflammation, we verified the role of metal hypersensitivity by patch testing (PT) and lymphocyte transformation test (LTT). Methods:, In the 16 patients with lymphocyte dominated periprosthetic inflammation, allergy history was obtained by a questionnaire, specific serum IgE to aeroallergens was measured to assess atopy, PT to standard and metal series was performed and metal sensitivity was further assessed by LTT using blood mononuclear cells. Results:, Revision surgery was performed because of pain (8/16), osteolysis (4/16), dislocation (3/16) and loosening of the stem (1/16). Histological examination showed perivascular infiltrates of T lymphocytes, high endothelial venules, fibrin exudation and accumulation of macrophages with drop-like inclusions. Five patients had a history of cutaneous metal allergy and atopy was found in 25% of the patients. In 13/16 patients (81%), systemic metal sensitivity was found based on PT and/or LTT. Patch test reactions were seen in 11/16 patients (69%; partly multiple reactions/patient): 7/16 to Cobalt (Co), 7/16 to Chromium (Cr), 4/16 to Nickel (Ni), and one each to Molybdenum (Mo) and Manganese (Mn). Ten of 16 patients (62%) showed enhanced LTT reactivity to metals: 7/16 to Ni, 7/16 to Co, 5/16 to Cr, 5/16 to Mo and 4/16 to Mn. Conclusions:, The lymphocyte dominated peri-implant inflammation may well reflect an allergic hyper-reactivity in these patients, given the high rate of concomitantly found metal allergy. Despite the overall incidence of metal implant allergy being low, allergic reactions should be included as differential diagnosis in failed metal-on-metal arthroplasty. [source]

Axillary perifollicular xanthomatosis resembling Fox,Fordyce disease

AUSTRALASIAN JOURNAL OF DERMATOLOGY, Issue 2 2004
Steven Kossard
SUMMARY A 40-year-old woman presented with a 2-year history of intermittently pruritic pale yellow follicular papules localized to both axillae associated with decreased axillary hair growth and sweating. Skin biopsies revealed an expanded perifollicular adventitial sheath packed with xanthoma cells. There was scant lymphocytic inflammation around the follicles. Vacuolated keratinocytes were present within the infundibular region of the follicles. Serum lipid levels and serum protein electrophoresis were both normal. The features in our case overlap those described recently as a xanthomatous variant of Fox,Fordyce disease. However, in our patient the pruritus was not intense, the lesions were confined to the axillae, and the histopathological features of Fox,Fordyce disease were not confirmed. We prefer to classify our case as an axillary perifollicular xanthomatosis. It is possible that axillary perifollicular xanthomatosis is the follicular counterpart of the epidermal-based verruciform xanthomas, as both are normolipaemic and are limited to the adventitial tissue close to keratinocytes that may be the source of lipid. The finding of vacuolated keratinocytes in the infundibular region in our case may support this mechanism. [source]