Tumour necrosis factor α augments the inhibitory effects of CTLA-4-Ig on osteoclast generation from human monocytes via induction of CD80 expression.


Journal

Clinical and experimental immunology
ISSN: 1365-2249
Titre abrégé: Clin Exp Immunol
Pays: England
ID NLM: 0057202

Informations de publication

Date de publication:
06 2019
Historique:
accepted: 21 01 2019
pubmed: 7 2 2019
medline: 4 4 2020
entrez: 7 2 2019
Statut: ppublish

Résumé

Cytotoxic T lymphocyte antigen-4-immunoglobulin (CTLA-4-Ig) exerts anti-rheumatic action via negative regulation of the co-stimulation process between antigen-presenting cells and T cells. CTLA-4-Ig also binds to CD80/CD86 on monocytes of osteoclast precursors. However, little is known about the effect of CTLA-4-Ig on osteoclastogenesis in rheumatoid arthritis (RA). In this study we evaluated the effects of CTLA-4-Ig on osteoclast generation from human blood monocytes (PBM) and rheumatoid synovial fluid monocytes (RSFM). Highly purified monocytes were cultured with receptor activator of nuclear factor kappa-B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) in the presence of CTLA-4-Ig. CTLA-4-Ig inhibited RANKL-induced osteoclast generation in PBM and RSFM, as determined by tartrate-resistant acid phosphatase (TRAP) staining and bone resorption assay using osteo assay surface plates. In addition, CTLA-4-Ig reduced the gene and protein expressions of nuclear factor of activated T cells, cytoplasmic 1 (NFATc1) and cathepsin K during osteoclastogenesis. Furthermore, CTLA-4-Ig significantly inhibited cell proliferation during osteoclastogenesis. Interestingly, the gene expression of indoleamine 2,3-dioxygenase-1, an inducer of apoptosis, was enhanced by CTLA-4-Ig. We next examined the effect of tumour necrosis factor (TNF)-α, a major inflammatory cytokine in rheumatoid synovium, on the expression of CD80 and CD86 by flow cytometric analysis. TNF-α potently induced the surface expression of CD80, which is known to have much higher affinity to CTLA-4-Ig than CD86, and this induction was observed at mRNA levels. Interestingly, freshly prepared rheumatoid synovial monocytes also expressed CD80 as much as TNF-α-treated PBM. Furthermore, TNF-α enhanced CTLA-4-Ig-induced inhibition of osteoclastogenesis and cell proliferation. Taken together, the TNF-α-induced CD80 may augment CTLA-4-Ig-induced inhibition of osteoclastogenesis, suggesting that CTLA-4-Ig potently inhibits osteoclast differentiation and protects bone destruction in rheumatoid inflamed joints.

Identifiants

pubmed: 30724348
doi: 10.1111/cei.13271
pmc: PMC6514374
doi:

Substances chimiques

B7-1 Antigen 0
Tumor Necrosis Factor-alpha 0
Abatacept 7D0YB67S97

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

392-402

Informations de copyright

© 2019 British Society for Immunology.

Références

Arthritis Rheum. 2000 Feb;43(2):250-8
pubmed: 10693863
Arthritis Rheum. 2000 Feb;43(2):259-69
pubmed: 10693864
J Immunol. 2001 Jul 1;167(1):140-6
pubmed: 11418642
Immunity. 2002 Aug;17(2):201-10
pubmed: 12196291
Cell Death Differ. 2002 Oct;9(10):1069-77
pubmed: 12232795
Immunity. 2006 Mar;24(3):233-8
pubmed: 16546089
Cell Immunol. 1991 Oct 15;137(2):429-37
pubmed: 1716521
Ann Rheum Dis. 2008 Nov;67(11):1603-9
pubmed: 18203760
Immunol Rev. 2009 May;229(1):307-21
pubmed: 19426230
Nat Rev Rheumatol. 2009 Dec;5(12):667-76
pubmed: 19884898
Arthritis Res Ther. 2009;11(6):R176
pubmed: 19930661
Nat Rev Immunol. 2011 Nov 25;11(12):852-63
pubmed: 22116087
N Engl J Med. 2011 Dec 8;365(23):2205-19
pubmed: 22150039
Arthritis Rheum. 2013 Jan;65(1):28-38
pubmed: 23169319
Sci Transl Med. 2014 May 7;6(235):235ra60
pubmed: 24807557
Ann Rheum Dis. 2016 Apr;75(4):709-14
pubmed: 26359449
Arthritis Rheum. 1994 Nov;37(11):1637-46
pubmed: 7526869
Cell Immunol. 1995 Apr 1;161(2):226-35
pubmed: 7535196
Immunology. 1996 Dec;89(4):592-8
pubmed: 9014827
J Immunol. 1999 Feb 15;162(4):1947-51
pubmed: 9973463

Auteurs

K Oi (K)

Department of Clinical Immunology and Rheumatology, Hiroshima University Hospital, Hiroshima, Japan.

T Tokunaga (T)

Department of Clinical Immunology and Rheumatology, Hiroshima University Hospital, Hiroshima, Japan.

T Kuranobu (T)

Department of Clinical Immunology and Rheumatology, Hiroshima University Hospital, Hiroshima, Japan.

K Yukawa (K)

Department of Clinical Immunology and Rheumatology, Hiroshima University Hospital, Hiroshima, Japan.

H Kohno (H)

Department of Clinical Immunology and Rheumatology, Hiroshima University Hospital, Hiroshima, Japan.

Y Yoshida (Y)

Department of Clinical Immunology and Rheumatology, Hiroshima University Hospital, Hiroshima, Japan.

S Mokuda (S)

Department of Clinical Immunology and Rheumatology, Hiroshima University Hospital, Hiroshima, Japan.

S Hirata (S)

Department of Clinical Immunology and Rheumatology, Hiroshima University Hospital, Hiroshima, Japan.

E Sugiyama (E)

Department of Clinical Immunology and Rheumatology, Hiroshima University Hospital, Hiroshima, Japan.

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