Fas Ligand Elicits a Caspase-Independent Proinflammatory Response in Human Keratinocytes: Implications for Dermatitis
- 1 November 2006
- journal article
- Published by Elsevier BV in Journal of Investigative Dermatology
- Vol. 126 (11), 2438-2451
- https://doi.org/10.1038/sj.jid.5700477
Abstract
No abstract availableKeywords
This publication has 50 references indexed in Scilit:
- Identification of NF-κB-regulated genes induced by TNFα utilizing expression profiling and RNA interferenceOncogene, 2003
- The UV (Ribotoxic) Stress Response of Human Keratinocytes Involves the Unexpected Uncoupling of the Ras-Extracellular Signal-Regulated Kinase Signaling Cascade from the Activated Epidermal Growth Factor ReceptorMolecular and Cellular Biology, 2002
- Keratinocytes from patients with atopic dermatitis and psoriasis show a distinct chemokine production profile in response to T cell–derived cytokinesJournal of Allergy and Clinical Immunology, 2001
- Fas (CD95) Induces Alveolar Epithelial Cell Apoptosis in VivoThe American Journal of Pathology, 2001
- T cell–mediated Fas-induced keratinocyte apoptosis plays a key pathogenetic role in eczematous dermatitisJCI Insight, 2000
- An Induced Proximity Model for Caspase-8 ActivationPublished by Elsevier BV ,1998
- Apoptosis is the mode of keratinocyte death in cutaneous graft-versus-host diseaseJournal of the American Academy of Dermatology, 1996
- FLICE, A Novel FADD-Homologous ICE/CED-3–like Protease, Is Recruited to the CD95 (Fas/APO-1) Death-Inducing Signaling ComplexCell, 1996
- Involvement of MACH, a Novel MORT1/FADD-Interacting Protease, in Fas/APO-1- and TNF Receptor–Induced Cell DeathCell, 1996
- A role for CD95 ligand in preventing graft rejectionNature, 1995