ArticleThe American journal of pathology2005
The contribution of the Fas/FasL apoptotic pathway in ulcer formation during Leishmania major-induced cutaneous Leishmaniasis.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 37 citations in OpenAlex.
- Dysregulation of caspase-8 and caspase-9 in T-lymphocyte apoptosis: implications for pathogenesis, diagnosis, and therapeutic targeting in psoriatic arthritis.BMC molecular and cell biology · 2026Article
- The Impact of Neutrophil Recruitment to the Skin on the Pathology Induced byFrontiers in immunology · 2021Review
- Activity of synthetic chalcones in hamsters experimentally infected with Leishmania (Viannia) braziliensis.Parasitology research · 2015Article
- Inhibition of caspase-8 activity promotes protective Th1- and Th2-mediated immunity to Leishmania major infection.Journal of leukocyte biology · 2014Article
- FasL and TRAIL signaling in the skin during cutaneous leishmaniasis - implications for tissue immunopathology and infectious control.Frontiers in immunology · 2012Article
- Apoptosis induced by parasitic diseases.Parasites & vectors · 2010Article
- Systemic FasL and TRAIL neutralisation reduce leishmaniasis induced skin ulceration.PLoS neglected tropical diseases · 2010Article
- Immunological perspectives of leishmaniasis.Journal of global infectious diseases · 2010Article
- Caspase-8 deficiency in epidermal keratinocytes triggers an inflammatory skin disease.The Journal of experimental medicine · 2009Article
- Recent developments leading toward a paradigm switch in the diagnostic and therapeutic approach to human leishmaniasis.Current opinion in infectious diseases · 2008Review
- FasL and TRAIL induce epidermal apoptosis and skin ulceration upon exposure to Leishmania major.The American journal of pathology · 2007Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
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Abstract
Cutaneous leishmaniasis (CL), caused by the intracellular protozoan Leishmania major, is characterized by lesion formation and ulceration at the site of infection. The mechanism of ulcer formation during CL is not fully understood. The expression of Fas and FasL and the levels of apoptosis in skin biopsies and in restimulated blood mononuclear cells from patients with 1 to 7 months of L. major-induced CL were analyzed using immunohistochemistry and fluorescence-activated cell sorting analysis. The levels of soluble Fas and FasL were also analyzed by enzyme-linked immunosorbent assay. A substantial number of apoptotic keratinocytes were observed mainly in the superficial epidermis of morphologically active and healing CL skin samples. Fas expression was increased on epidermis in active CL, whereas Fas expression was similar in healing and healthy epidermis. FasL-expressing macrophages and T cells were found in subepidermal infiltrate, mainly in active disease. When CL peripheral blood mononuclear cells were restimulated with L. major, Fas was up-regulated on effector T cells, and high levels of sFasL were secreted. Supernatants from restimulated cultures induced apoptosis in human keratinocytes (HaCaT), possibly through Fas/FasL interactions. Our results indicate that FasL-expressing effector T cells and macrophages may act to induce apoptosis and ulcer formation in Fas-expressing keratinocytes during L. major infection.
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