Eczematous dermatitis

About: Eczematous dermatitis is a research topic. Over the lifetime, 704 publications have been published within this topic receiving 12832 citations.

Pedigree demonstrating a sex-linked recessive condition characterized by draining ears, eczematoid dermatitis and bloody diarrhea.

Abstract: Genetic analysis of the family of an individual suffering from what appeared to be secondary thrombocytopenic purpura indictated that: 1. Sixteen of 40 male infants died. 2. Ten of these, including the proband, were known to have suffered from draining ears, eczematoid dermatitis and bloody diarrhea. 3. The pattern of deaths agrees with the assumption that a sex-linked recessive gene is responsible for the primary deviation which leads to the death of these infants.

T cell-mediated Fas-induced keratinocyte apoptosis plays a key pathogenetic role in eczematous dermatitis.

Abstract: Clinical and histologic similarities between various eczematous disorders point to a common efferent pathway. We demonstrate here that activated T cells infiltrating the skin in atopic dermatitis (AD) and allergic contact dermatitis (ACD) induce keratinocyte (KC) apoptosis. KCs normally express low levels of Fas receptor (FasR) that can be substantially enhanced by the presence of IFN-γ. KCs are rendered susceptible to apoptosis by IFN-γ when FasR numbers reach a threshold of approximately 40,000 per KC. Subsequently, KCs undergo apoptosis induced by anti-FasR mAb’s, soluble Fas ligand, supernatants from activated T cells, or direct contact between T cells and KCs. Apoptotic KCs show typical DNA fragmentation and membrane phosphatidylserine expression. KC apoptosis was demonstrated in situ in lesional skin affected by AD, ACD, and patch tests. Using numerous cytokines and anti-cytokine neutralizing mAb’s, we found no evidence that cytokines other than IFN-γ participate in this process. In addition, apoptosis-inducing pathways other than FasR triggering were ruled out by blocking T cell–induced KC apoptosis by caspase inhibitors and soluble Fas-Fc protein. Responses of normal human skin and cultured skin equivalents to activated T cells demonstrated that KC apoptosis caused by skin-infiltrating T cells is a key event in the pathogenesis of eczematous dermatitis.

A glucagon-secreting alpha-cell carcinoma of the pancreas.

Abstract: TUMORS of the islands of Langerhans have been associated with three distinct entities: hyperinsulinism; the nlcerogenie Zollinger – Ellison syndrome; and a syndrome of diarrhea unassociated with gastric hypersecretion. This report documents a fourth type of humoral activity, that of hyperglucagonism, associated with an alpha-cell carcinoma of the pancreatic islets. It is probable that cases of this disorder are at present unrecognized, or classified otherwise. Therefore, the clinical, laboratory and cytologic findings whereby this condition may be identified are set forth. Case Report A 42-year-old housewife was first seen in February, 1963, because of a bullous and eczematoid dermatitis of . . .

Th2-like CD8+ T cells showing B cell helper function and reduced cytolytic activity in human immunodeficiency virus type 1 infection.

Abstract: We analyzed at clonal level the functional profile of circulating or skin-infiltrating T lymphocytes from two individuals infected with the human immunodeficiency virus type 1 (HIV-1), suffering from a Job's-like syndrome (eczematous dermatitis, recurrent skin and sinopulmonary infections, and hypergammaglobulinemia E) and showing virtually no circulating CD4+ T cells. Most of the CD3+ T cell clones generated from both patients were CD4- CD8+ TCR alpha beta +. The others were CD4- CD8- TCR alpha beta + which exhibited reduced mRNA expression for the CD8 molecule or no mRNA expression for either CD4 or CD8 molecules. The great majority of both CD4- CD8+ and CD4- CD8- did not produce interferon (IFN) gamma and exhibited reduced cytolytic activity. Rather, most of them produced large amounts of both interleukin (IL) 4 and IL-5 and provided B cell helper function for IgE synthesis. These data suggest that a switch of cytolytic CD8+ T cells showing a Th1-like cytokine secretion profile to cells that make Th2-type cytokines, exhibit reduced cytolytic potential, and provide B cell helper function can occur in the course of HIV-1 infection. These cells may contribute to the reduced defense against viral infections and intracellular parasites and account for the elevated IgE serum levels, eosinophilia, and the allergic-like clinical manifestations seen in a proportion of HIV-1-infected individuals.