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Blood, Vol. 95 No. 4 (February 15), 2000:
pp. 1378-1385
Gene expressions of lipopolysaccharide receptors, toll-like
receptors 2 and 4, are differently regulated in mouse T lymphocytes
Tetsuya Matsuguchi,
Kensuke Takagi,
Tipayaratn Musikacharoen, and
Yasunobu Yoshikai
From the Laboratory of Host Defense and Germfree Life, Research
Institute for Disease Mechanism and Control, Nagoya University School
of Medicine, Nagoya, Japan.
Toll-like receptors (TLRs) are a family of mammalian proteins
homologous to Drosophila Toll. Human TLR2 was
shown to mediate the responsiveness to lipopolysaccharide (LPS). On the
other hand, gene mutations of mouse TLR4 (mTLR4) in LPS-hyporesponsive
strains have suggested that mTLR4 is essential for LPS-signaling in
mice, but the role of mTLR2 has not been explored. This report
describes molecular cloning of the mTLR2 cDNA. Overexpression of mTLR2
and mouse CD14 conferred LPS-inducibility of c-Jun N-terminal kinase phosphorylation and nuclear factor- B activation to COS7 cells, suggesting that mTLR2 is a signaling receptor for LPS. Both
mTLR2 and mTLR4 genes were expressed in T cells.
Treatment with anti-CD3 , PMA plus ionomycin, or interleukin-2
(IL-2)/IL-15 increased mTLR2 but not mTLR4 messenger RNA (mRNA) in some
T cell lines. Specific inhibitors of mitogen-activated extracellular
signal-regulated kinase and fusion protein 38 (p38) kinase inhibited
mTLR2 mRNA up-regulation by PMA plus ionomycin. This suggests that
extracellular signal-regulated kinase and p38 kinase pathways were
involved. Additionally, LPS treatment of EL-4 cell line decreased
IL-4 gene expression. Our results indicate that both mTLR2 and
mTLR4 are involved in LPS signaling, but their expressions are
regulated differently in T cells, and that LPS may directly affect
T-cell functions by binding to TLRs.
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