scholarly journals Inhibition of Tumor Progression Locus 2 Protein Kinase Suppresses Receptor Activator of Nuclear Factor-κB Ligand-Induced Osteoclastogenesis through Down-Regulation of the c-Fos and Nuclear Factor of Activated T Cells c1 Genes

2010 ◽  
Vol 33 (1) ◽  
pp. 133-137 ◽  
Author(s):  
Kazuya Hirata ◽  
Hirofumi Taki ◽  
Kouichiro Shinoda ◽  
Hiroyuki Hounoki ◽  
Tatsuro Miyahara ◽  
...  
Keyword(s):  
T Cells ◽  
Protein Kinase ◽  
Tumor Progression ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Down Regulation ◽  
Activated T Cells ◽  
Receptor Activator

scholarly journals Protein Kinase Cζ Phosphorylates Nuclear Factor of Activated T Cells and Regulates Its Transactivating Activity

2002 ◽  
Vol 277 (30) ◽  
pp. 27073-27080 ◽  
Author(s):  
Belén San-Antonio ◽  
Miguel A. Íñiguez ◽  
Manuel Fresno
Keyword(s):  
T Cells ◽  
Protein Kinase ◽  
Nuclear Factor ◽  
Activated T Cells

Human myeloma cells stimulate the receptor activator of nuclear factor-κB ligand (RANKL) in T lymphocytes: a potential role in multiple myeloma bone disease

Blood ◽  
2002 ◽  
Vol 100 (13) ◽  
pp. 4615-4621 ◽  
Author(s):  
Nicola Giuliani ◽  
Simona Colla ◽  
Roberto Sala ◽  
Matteo Moroni ◽  
Mirca Lazzaretti ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
T Cells ◽  
T Lymphocytes ◽  
Bone Disease ◽  
Nuclear Factor Κb ◽  
Myeloma Cell ◽  
Nuclear Factor ◽  
Free System ◽  
Receptor Activator ◽  
Ifn Γ

The biologic mechanisms involved in the pathogenesis of multiple myeloma (MM) bone disease are not completely understood. Recent evidence suggests that T cells may regulate bone resorption through the cross-talk between the critical osteoclastogenetic factor, receptor activator of nuclear factor-κB ligand (RANKL), and interferon γ (IFN-γ) that strongly suppresses osteoclastogenesis. Using a coculture transwell system we found that human myeloma cell lines (HMCLs) increased the expression and secretion of RANKL in activated T lymphocytes and similarly purified MM cells stimulated RANKL production in autologous T lymphocytes. In addition, either anti–interleukin 6 (anti–IL-6) or anti–IL-7 antibody inhibited HMCL-induced RANKL overexpression. Consistently, we demonstrated that HMCLs and fresh MM cells express IL-7 mRNA and secrete IL-7 in the presence of IL-6 and that bone marrow (BM) IL-7 levels were significantly higher in patients with MM. Moreover, we found that the release of IFN-γ by T lymphocytes was reduced in presence of both HMCLs and purified MM cells. Furthermore, in a stromal cell–free system, osteoclastogenesis was stimulated by conditioned medium of T cells cocultured with HMCLs and inhibited by recombinant human osteoprotegerin (OPG; 100 ng/mL to 1 μg/mL). Finally, RANKL mRNA was up-regulated in BM T lymphocytes of MM patients with severe osteolytic lesions, suggesting that T cells could be involved at least in part in MM-induced osteolysis through the RANKL overexpression.

B-cell antigen receptor activates transcription factors NFAT (nuclear factor of activated T-cells) and NF-κB (nuclear factor κB) via a mechanism that involves diacylglycerol

2004 ◽  
Vol 32 (1) ◽  
pp. 113-115 ◽  
Author(s):  
P. Antony ◽  
J.B. Petro ◽  
G. Carlesso ◽  
N.P. Shinners ◽  
J. Lowe ◽  
...  
Keyword(s):  
T Cells ◽  
Transcription Factors ◽  
B Cell ◽  
Antigen Receptor ◽  
Nuclear Factor Κb ◽  
B Cell Antigen Receptor ◽  
Nuclear Factor ◽  
Activated T Cells ◽  
Cell Antigen Receptor ◽  
Cell Antigen

Engagement of the B-cell antigen receptor (BCR) induces the activation of various transcription factors, including NFAT (nuclear factor of activated T-cells) and NF-κB (nuclear factor κB), which participate in long-term biological responses such as proliferation, survival and differentiation of B-lymphocytes. We addressed the biochemical basis of this process using the DT40 chicken B-cell lymphoma. We discovered that Bruton's tyrosine kinase (BTK) and phospholipase C-γ2 (PLC-γ2) are required to activate NFAT and NF-κB, and to produce the lipid second messenger diacylglycerol in response to BCR cross-linking. Therefore the functional integrity of the BTK/PLC-γ2/diacylglycerol signalling axis is crucial for BCR-directed activation of both transcription factors NFAT and NF-κB.

Sign in / Sign up

Export Citation Format

Share Document