Author
M. Lohoff
Bio: M. Lohoff is an academic researcher. The author has contributed to research in topics: Autoimmunity. The author has an hindex of 1, co-authored 1 publications receiving 1194 citations.
Topics: Autoimmunity
Papers
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01 Jan 1995
TL;DR: Fas expression and function were analyzed in three children with a lymphoproliferative syndrome and may provide a molecular basis for some autoimmune diseases in humans.
Abstract: Fas (also known as Apo1 and CD95) is a cell surface receptor involved in apoptotic cell death. Fas expression and function were analyzed in three children (including two siblings) with a lymphoproliferative syndrome, two of whom also had autoimmune disorders. A large deletion in the gene encoding Fas and no detectable cell surface expression characterized the most affected patient. Clinical manifestations in the two related patients were less severe: Fas-mediated apoptosis was impaired and a deletion within the intracytoplasmic domain was detected. These findings illustrate the crucial regulatory role of Fas and may provide a molecular basis for some autoimmune diseases in humans.
1,194 citations
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TL;DR: This work was supported in part by Grants-in-Aid from the Ministry of Education, Science, and Culture of Japan and by a Research Grant from the Princess Takamatsu Cancer Research Fund, and performed in part through Special Coordination Funds of the Science and Technology Agency of the Japanese Government.
5,054 citations
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TL;DR: The authors regret the inability to cite all of the primary literature contributing to this review due to length considerations, but wish to thank F. Chan, T. Migone, and J. Wang for insightful comments on the manuscript.
3,756 citations
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TL;DR: A novel tumor necrosis factor (TNF) family member has been cloned and characterized, and the TRAIL gene is located on chromosome 3 at position 3q26, which is not close to any other known TNF ligand family members.
2,996 citations
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TL;DR: The role of CD95 (Apo-1/Fas)-mediated signalling in T-cell and B-cell development and during the course of an immune response and the understanding of the pathogenesis of diseases such as cancer, autoimmunity and AIDS is improved.
Abstract: Apoptosis in the immune system is a fundamental process regulating lymphocyte maturation, receptor repertoire selection and homeostasis Thus, death by apoptosis is as essential for the function of lymphocytes as growth and differentiation This article focuses on death receptor-associated apoptosis and the role of CD95 (Apo-1/Fas)-mediated signalling in T-cell and B-cell development and during the course of an immune response Gaining an insight into these processes improves our understanding of the pathogenesis of diseases such as cancer, autoimmunity and AIDS, and opens new approaches to rational treatment strategies
1,721 citations
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TL;DR: Tumor necrosis factor and lymphotoxin-α were isolated more than 10 years ago on the basis of their ability to kill tumor cells in vitro and to cause hemorrhagic necrosis of transplantable tumors in mice, and a factor known as cachectin was isolated from mouse macrophages, sequenced, and shown to be identical to TNF.
Abstract: Tumor necrosis factor (TNF) and lymphotoxin-α were isolated more than 10 years ago, on the basis of their ability to kill tumor cells in vitro and to cause hemorrhagic necrosis of transplantable tumors in mice.1 The complementary DNAs and genes encoding each protein were cloned immediately thereafter.2,3 Concurrently, a factor known as cachectin was isolated from mouse macrophages, sequenced, and shown to be identical to TNF.4,5 Cachectin was identified not as a cytolysin, but as a catabolic hormone that suppressed the expression of lipoprotein lipase and other anabolic enzymes in fat.6–8 Still other studies demonstrated the powerful . . .
1,248 citations