ArticleThe Journal of experimental medicine1998
Challenging cytokine redundancy: inflammatory cell movement and clinical course of experimental autoimmune encephalomyelitis are normal in lymphotoxin-deficient, but not tumor necrosis factor-deficient, mice.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
48 citing papers in PubMed, 164 citations in OpenAlex.
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- Early CCR6 expression on B cells modulates germinal centre kinetics and efficient antibody responses.Immunology and cell biology · 2017Article
- IL-1β Is Involved with the Generation of Pain in Experimental Autoimmune Encephalomyelitis.Molecular neurobiology · 2016Article
- TNF-Mediated Restriction of Arginase 1 Expression in Myeloid Cells Triggers Type 2 NO Synthase Activity at the Site of Infection.Cell reports · 2016Article
- Design of oral agents for the management of multiple sclerosis: benefit and risk assessment for dimethyl fumarate.Drug design, development and therapy · 2014Review
- The contribution of immune and glial cell types in experimental autoimmune encephalomyelitis and multiple sclerosis.Multiple sclerosis international · 2014Review
- The experimental autoimmune encephalomyelitis (EAE) model of MS: utility for understanding disease pathophysiology and treatment.Handbook of clinical neurology · 2014Review
- Placenta suppresses experimental autoimmune hypophysitis through soluble TNF receptor 1.Journal of autoimmunity · 2012Article
- Tumour necrosis factor-mediated macrophage activation in the target organ is critical for clinical manifestation of uveitis.Clinical and experimental immunology · 2012Article
- Pathogenic CD8 T cells in multiple sclerosis and its experimental models.Frontiers in immunology · 2012Article
- Lymphotoxin signals from positively selected thymocytes regulate the terminal differentiation of medullary thymic epithelial cells.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Expression of astrocytic type 2 angiotensin receptor in central nervous system inflammation correlates with blood-brain barrier breakdown.Journal of molecular neuroscience : MN · 2010Article
- Gammadelta T cells in EAE: early trafficking events and cytokine requirements.European journal of immunology · 2009Article
- Lymphotoxin-alpha and TNF have essential but independent roles in the evolution of the granulomatous response in experimental leprosy.The American journal of pathology · 2009Article
- Transgenic inhibition of astroglial NF-kappa B improves functional outcome in experimental autoimmune encephalomyelitis by suppressing chronic central nervous system inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- An ENU-induced mutation in the lymphotoxin alpha gene impairs organogenesis of lymphoid tissues in C57BL/6 mice.Biochemical and biophysical research communications · 2008Article
- The lymphotoxin pathway regulates Aire-independent expression of ectopic genes and chemokines in thymic stromal cells.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- RANK signals from CD4(+)3(-) inducer cells regulate development of Aire-expressing epithelial cells in the thymic medulla.The Journal of experimental medicine · 2007Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lymphotoxin (LT) is widely regarded as a proinflammatory cytokine with activities equivalent to tumor necrosis factor (TNF). The contribution of LT to experimental autoimmune encephalomyelitis (EAE) was examined using TNF/LTalpha-/- mice, TNF-/- mice, and a new LTalpha-/- line described here. All mice were generated directly in the C57BL/6 strain and used for the preparation of radiation bone marrow chimeras to reconstitute peripheral lymphoid organs and restore immunocompetence. This approach overcame the problems related to the lack of lymph nodes that results from LTalpha gene targeting. We show here that when LT is absent but TNF is present, EAE progresses normally. In contrast, when TNF is absent but LT is present, EAE is delayed in onset and inflammatory leukocytes fail to move normally into the central nervous system parenchyma, even at the peak of disease. In the absence of both cytokines, the clinical and histological picture is identical to that seen when TNF alone is deficient, including demyelination. Furthermore, the therapeutic inhibition of TNF and LTalpha with soluble TNF receptor in unmanipulated wild-type or TNF-/- mice exactly reproduces these outcomes. We conclude from these studies that TNF and LT are functionally distinct cytokines in vivo, and despite sharing common receptors, show no redundancy of function nor mutual compensation.
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