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Antibodies 2015, 4(1), 1-10; doi:10.3390/antib4010001

Both Tumor Necrosis Factor Receptor Signaling Pathways Contribute to Mortality but not to Splenomegaly in Generalized Lymphoproliferative Disorder

1
Comparative Genomics Centre, James Cook University, Townsville, Qld 4811, Australia
2
Heinrich Körner, Menzies Research Institute Tasmania, Medical Science 2, 17 Liverpool Street, Hobart, Tasmania 7000, Australia
Current address: Cellular Signaling and Human Disease Laboratory, Department of Biochemistry & Molecular Biology, Monash University, VIC 3800, Australia.
Current address: Klinik und Poliklinik für Neurologie, Johannes Gutenberg-Universität, D-55131 Mainz, Germany.
*
Author to whom correspondence should be addressed.
Academic Editor: Dimiter S. Dimitrov
Received: 12 September 2014 / Accepted: 10 December 2014 / Published: 24 December 2014
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Abstract

The phenotypical consequences of a combined deficiency of the Fas-Fas Ligand (FasL) and one or both Tumor Necrosis Factor (TNF) signaling pathways were investigated. Mice, which expressed a non-functional FasL suffered from a pathological accumulation of both B and T cells leading to splenomegaly and lymphadenopathy and, depending on the genetic background, pathogenic self-reactive antibodies (generalized lymphoproliferative disorder (gld)-phenotype). If mice additionally lacked TNF, they displayed a significantly ameliorated gld-phenotype while TNF Receptor-1-deficient gld mice (B6.gld.TNFR1−/−) displayed a more severe phenotype. To complement this combination, we also generated TNF Receptor-2-deficient gld mice (B6.gld.TNFR2−/−). Both double knockouts followed in their splenic structure the respective TNFR contribution to the phenotype. TNFR1−/− mice showed an absence of B cell follicles in the spleen while TNFR2−/− mice were comparable to WT mice. In general, we demonstrated a strong contribution of both TNFR signaling pathways to the symptoms of gld with the notable exception of splenomegaly where only TNFR1−/− played a role. View Full-Text
Keywords: autoimmunity; tumor necrosis factor; tumor necrosis factor receptor; gene-deficient models autoimmunity; tumor necrosis factor; tumor necrosis factor receptor; gene-deficient models
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Wiede, F.; Roomberg, A.; Darby, J.; Gollan, R.; Körner, H. Both Tumor Necrosis Factor Receptor Signaling Pathways Contribute to Mortality but not to Splenomegaly in Generalized Lymphoproliferative Disorder. Antibodies 2015, 4, 1-10.

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