ABSTRACT
Background: langerhans cells are important in the pathogenesis of leprosy. A recent study reported that these cells were almost absent in the epidermis overlying lepromatous lesions
Objective: to investigate a possible relationship between the number of Langerhans cells and the histopathologic spectrum of lesions in patients with leprosy
Methods: an immunohistochemical staining for S100 protein was used to study skin punch biopsies of patients with leprosy and to quantify S100-positive Langerhans cells in the epidermis
Results: a progressively significant reduction in the number of Langerhans cells was found from tuberculoid to lepromatous skin lesions. Langerhans cells were significantly less frequent in lepromatous and borderline lepromatous as compared to either tuberculoid or borderline tuberculoid leprosy
Conclusion: in view of the fact that adequate numbers of dendritic cells are recruited to the dermis, their maturation/ migration to Langerhans cells in the epidermis is impaired in lepromatous leprosy
Subject(s)
Humans , Male , Female , Helicobacter pylori/pathogenicity , Gastritis/pathology , GastroscopyABSTRACT
Rhinosporidiosis is a chronic granulomatous disease primarily of the anterior nares. It is histologically characterized by mucosal lymphoplasmacellular infiltrates, transepithelial elimination of nodular bodies [NB] and destruction of late stage NBs in histiocytic granulomata with central neutrophilic microabscesses. Early NBs are immunohistochemically positive for alpha 1-AT alpha 1-ACT, CEA, S100, fibronectin, amyloid-p-component, IgG, IgA, Clq and C3. Structures formerly regarded as "sporangia" [NB] and "spores" are believed to be lysosomal bodies loaded with indigestible residues to be cleared via transepithelial elimination. This is supported by immunohistochemical findings and ultrastructural demonstration of lysosomal bodies in early NBs but not in end-stage NBs which contain mostly amorphous electron dense materials. Immunopathology of the disease is discussed and in view of overwhelming evidence against a fungal etiology it is proposed to change the name to Seeber's disease