scholarly journals Lymphotoxin-α and TNF Have Essential but Independent Roles in the Evolution of the Granulomatous Response in Experimental Leprosy

2009 ◽  
Vol 174 (4) ◽  
pp. 1379-1389 ◽  
Author(s):  
Deanna A. Hagge ◽  
Bernadette M. Saunders ◽  
Gigi J. Ebenezer ◽  
Nashone A. Ray ◽  
Vilma T. Marks ◽  
...  
Keyword(s):  
Experimental Leprosy ◽  
Lymphotoxin Α ◽  
Granulomatous Response

scholarly journals The effect of HLA–DR on susceptibility to rheumatoid arthritis is influenced by the associated lymphotoxin α–tumor necrosis factor haplotype

2003 ◽  
Vol 48 (1) ◽  
pp. 90-96 ◽  
Author(s):  
Julia Newton ◽  
Matthew A. Brown ◽  
Anita Milicic ◽  
Hans Ackerman ◽  
Chris Darke ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Hla Dr ◽  
Lymphotoxin Α ◽  
Necrosis Factor

scholarly journals Mycobacterium leprae in ocular tissues: Histopathological findings in experimental leprosy

2011 ◽  
Vol 77 (2) ◽  
pp. 252 ◽  
Author(s):  
Patrícia Deps ◽  
JoãoM.A.P Antunes ◽  
Belone Andréa de F ◽  
PatríciaS Rosa ◽  
AdrianaV Cardozo
Keyword(s):  
Mycobacterium Leprae ◽  
Ocular Tissues ◽  
Histopathological Findings ◽  
Experimental Leprosy

Interactions of Lymphotoxin α (TNF-β), Angiotensin-Converting Enzyme (ACE), and Endothelin-1 (ET-1) Gene Polymorphisms in Adult Periodontitis

2001 ◽  
Vol 72 (1) ◽  
pp. 85-89 ◽  
Author(s):  
Lydie Izakovičová Hollá ◽  
Antonín Fassmann ◽  
Anna Vašků ◽  
Vladimír Znojil ◽  
Jiří Vaněk ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Gene Polymorphisms ◽  
Converting Enzyme ◽  
Endothelin 1 ◽  
Lymphotoxin Α

Experimental leprosy in three species of monkeys

Science ◽  
1985 ◽  
Vol 227 (4686) ◽  
pp. 529-531 ◽  
Author(s):  
R. Wolf ◽  
B. Gormus ◽  
L. Martin ◽  
G. Baskin ◽  
G. Walsh ◽  
...  
Keyword(s):  
Experimental Leprosy

scholarly journals Allele-specific repression of lymphotoxin-α by activated B cell factor-1

2004 ◽  
Vol 36 (4) ◽  
pp. 394-399 ◽  
Author(s):  
Julian C Knight ◽  
Brendan J Keating ◽  
Dominic P Kwiatkowski
Keyword(s):  
B Cell ◽  
Allele Specific ◽  
Lymphotoxin Α

scholarly journals Elevated lymphotoxin-α (TNFβ) is associated with intervertebral disc degeneration

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Zhu Guo ◽  
Chensheng Qiu ◽  
Christina Mecca ◽  
Yang Zhang ◽  
Jiang Bian ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Cell Viability ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Caspase 3 ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Optimal Conditions ◽  
Cell Degeneration ◽  
Lymphotoxin Α

Abstract Background Intervertebral disc degeneration (IVDD) is a primary cause of degenerative disc diseases; however, the mechanisms underlying the degeneration remain unclear. The immunoinflammatory response plays an important role in IVDD progression. The inflammatory cytokine lymphotoxin-α (LTα), formerly known as TNFβ, is associated with various pathological conditions, while its role in the pathogenesis of IVDD remains elusive. Methods Real-time quantitative polymerase chain reaction (RT-qPCR), Western blotting (WB), and enzyme-linked immunosorbent assays were used to assess the levels of LTα in human nucleus pulposus (NP) tissues between degeneration and control groups. The plasma concentrations of LTα and C-reactive protein (CRP) were compared between healthy and IVDD patients. Rat primary NP cells were cultured and identified via immunofluorescence. Methyl-thiazolyl-tetrazolium assays and flow cytometry were used to evaluate the effects of LTα on rat NP cell viability. After NP cells were treated with LTα, degeneration-related molecules (Caspase-3, Caspase-1, matrix metalloproteinase (MMP) -3, aggrecan and type II collagen) were measured via RT-qPCR and WB. Results The levels of both the mRNA and protein of LTα in human degenerated NP tissue significantly increased. Plasma LTα and CRP did not differ between healthy controls and IVDD patients. Rat primary NP cells were cultured, and the purity of primary NP cells was > 90%. Cell experiments showed inversely proportional relationships among the LTα dose, treatment time, and cell viability. The optimal conditions (dose and time) for LTα treatment to induce rat NP cell degeneration were 5 μg/ml and 48 ~ 72 h. The apoptosis rate and the levels of Caspase-3, Caspase-1, and MMP-3 significantly increased after LTα treatment, while the levels of type II collagen and aggrecan were decreased, and the protein expression levels were consistent with their mRNA expression levels. Conclusions This study demonstrated that elevated LTα is closely associated with IVDD and that LTα may induce NP cell apoptosis and reduce important extracellular matrix (ECM) proteins, which cause adverse effects on IVDD progress. Moreover, the optimal conditions for LTα treatment to induce NP cell degeneration were determined.

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