TY - JOUR
T1 - The role of lymphotoxin-α in rheumatoid arthritis
AU - Hirose, Tomohiro
AU - Fukuma, Yuri
AU - Takeshita, Ayumu
AU - Nishida, Keiichiro
N1 - Funding Information:
is a stockholder of Pfizer. KN has received research funding from Ab-bVie, Astellas, Chugai, Eisai, Mitsubishi-Tanabe, and Ono, and hono- raria from Astellas, Ayumi, Chugai, Mitsubishi-Tanabe, Pfizer, and Bristol-Myers Squibb/Ono. AT has no competing interests.
Funding Information:
Acknowledgements Medical writing support was provided by Helen Jones and Sabrina Giavara of Engage Scientific Solutions and was funded by Pfizer.
Funding Information:
Medical writing support was provided by Helen Jones and Sabrina Giavara of Engage Scientific Solutions and was funded by Pfizer. TH and YF are employees of Pfizer Japan Inc. TH is a stockholder of Pfizer. KN has received research funding from AbbVie, Astellas, Chugai, Eisai, Mitsubishi-Tanabe, and Ono, and honoraria from Astellas, Ayumi, Chugai, Mitsubishi-Tanabe, Pfizer, and Bristol-Myers Squibb/Ono. AT has no competing interests.
Publisher Copyright:
© 2018, Springer International Publishing AG, part of Springer Nature.
PY - 2018/6/1
Y1 - 2018/6/1
N2 - Background: The role of tumor necrosis factor (TNF) in the inflammatory response in rheumatoid arthritis (RA) is well established, whereas less is known about the role of TNF’s close homolog, lymphotoxin alpha (LTα). Findings: Increased levels of LTα are found in the serum and synovial tissue of patients with RA, and in vitro studies found that LTα-induced proliferation of RA fibroblast-like synoviocytes was at a similar level to TNF. These findings support the idea that anti-LTα treatment could be beneficial in patients with RA, but pateclizumab, an anti-LTα antibody, was not as efficacious as the anti-TNF agent adalimumab in reducing symptoms of RA in a head-to-head study, suggesting that anti-LTα therapies might not represent a valid alternative treatment option in patients with RA. However, suppression of LTα activity might be relevant in the context of RA-related comorbidities, as patients with RA have an increased risk of myocardial infarction (MI) compared with the general population, and specific polymorphisms of the LTα gene have been linked to increased MI risk. Conclusions: In this review, we summarize the key characteristics of LTα and the most recent findings on the role of LTα in RA.
AB - Background: The role of tumor necrosis factor (TNF) in the inflammatory response in rheumatoid arthritis (RA) is well established, whereas less is known about the role of TNF’s close homolog, lymphotoxin alpha (LTα). Findings: Increased levels of LTα are found in the serum and synovial tissue of patients with RA, and in vitro studies found that LTα-induced proliferation of RA fibroblast-like synoviocytes was at a similar level to TNF. These findings support the idea that anti-LTα treatment could be beneficial in patients with RA, but pateclizumab, an anti-LTα antibody, was not as efficacious as the anti-TNF agent adalimumab in reducing symptoms of RA in a head-to-head study, suggesting that anti-LTα therapies might not represent a valid alternative treatment option in patients with RA. However, suppression of LTα activity might be relevant in the context of RA-related comorbidities, as patients with RA have an increased risk of myocardial infarction (MI) compared with the general population, and specific polymorphisms of the LTα gene have been linked to increased MI risk. Conclusions: In this review, we summarize the key characteristics of LTα and the most recent findings on the role of LTα in RA.
KW - Etanercept
KW - Lymphotoxin alpha
KW - Pateclizumab
KW - Rheumatoid arthritis
KW - Tumor necrosis factor
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U2 - 10.1007/s00011-018-1139-6
DO - 10.1007/s00011-018-1139-6
M3 - Review article
C2 - 29541795
AN - SCOPUS:85043687303
VL - 67
SP - 495
EP - 501
JO - Inflammation Research
JF - Inflammation Research
SN - 1023-3830
IS - 6
ER -