Dermatophytosis is a cutaneous mycosis caused by a plethora of keratinophilic fungi, but Trichophyton rubrum is the most common etiological agent. Despite its high prevalence worldwide, little is known about the host defense mechanisms in this infection, particularly the in situ immune response. Using an immunohistochemistry approach, we investigated the density of CD1a+, factor XIIIa+ and CD68+ cells in the skin of dermatophytosis patients. Langerhans cells (CD1a+ cells) were significantly decreased in the epidermis of patients, both in affected and unaffected areas. In the dermis, however, no differences in the density of macrophages (CD68+ cells) and dermal dendrocytes (factor XIIIa+ cells) were observed. These results suggest that the decreased number of Langerhans cells may be a risk factor for development of dermatophytosis.
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http://dx.doi.org/10.1590/S1678-9946201961056 | DOI Listing |
Vestn Oftalmol
December 2024
Krasnov Research Institute of Eye Diseases, Moscow, Russia.
This lecture-format review presents a summary of methods for assessing the condition of corneal nerve fibers (CNF), their clinical significance, and an overview of their anatomy and physiology. It briefly analyzes the structural and functional characteristics of CNF in various ocular diseases, following eye surgeries, and in patients with systemic diseases accompanied by systemic polyneuropathy. The article describes in detail the management algorithm that involves a comprehensive analysis of CNF and Langerhans inflammatory cells, identifies the at-risk groups for developing structural nerve impairments, and outlines the main criteria for CNF assessment.
View Article and Find Full Text PDFExp Parasitol
December 2024
Romero Lascasas Porto Laboratory of Helminthology, Department of Microbiology, Immunology and Parasitology, Medical Sciences College (FCM), Rio de Janeiro State University (UERJ), Rio de Janeiro, Brazil.
It is not well understood how type 1 diabetes (T1D) and concomitant acute schistosomiasis mansoni affect pancreatic architecture. Male Swiss mice were administered streptozotocin (single 100 mg/kg i.p.
View Article and Find Full Text PDFJ Am Acad Dermatol
December 2024
Department of Dermatology, University of California Davis School of Medicine, Sacramento, CA; Department of Pathology and Laboratory Medicine, University of California Davis School of Medicine, Sacramento, CA. Electronic address:
Background: Allergic contact dermatitis cannot be reliably differentiated from other forms of spongiotic/eczematous dermatitis by histology alone. Textbooks and recent studies have variably supported the specificity of dermal eosinophils, eosinophilic spongiosis, and Langerhans cell collections, among other features.
Objective: To assess which histopathologic features favor a diagnosis of allergic contact dermatitis.
Cell
December 2024
Howard Hughes Medical Institute and Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143, USA. Electronic address:
Sustained lymphocyte migration from blood into lymph nodes (LNs) is important for immune responses. The CC-chemokine receptor-7 (CCR7) ligand CCL21 is required for LN entry but is downregulated during inflammation, and it has been unclear how recruitment is maintained. Here, we show that the oxysterol biosynthetic enzyme cholesterol-25-hydroxylase (Ch25h) is upregulated in LN high endothelial venules during viral infection.
View Article and Find Full Text PDFJCI Insight
December 2024
Department of Microbiology and Immunology, McGill University, Montreal, Quebec, Canada.
Deficits in IL-2 signaling can precipitate autoimmunity by altering the function and survival of FoxP3+ regulatory T cells (Tregs) while high concentrations of IL-2 fuel inflammatory responses. Recently, we showed that the non-beta IL-2 SYNTHORIN molecule SAR444336 (SAR'336) can bypass the induction of autoimmune and inflammatory responses by increasing its reliance on IL-2 receptor α chain subunit (CD25) to provide a bona fide IL-2 signal selectively to Tregs, making it an attractive approach for the control of autoimmunity. In this report, we further demonstrate that SAR'336 can support non-beta IL-2 signaling in murine Tregs and limit NK and CD8+ T cells' proliferation and function.
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