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논문 기본 정보

자료유형
학술저널
저자정보
저널정보
대한구강악안면외과학회 대한구강악안면외과학회지 대한구강악안면외과학회지 제36권 제6호
발행연도
2010.1
수록면
481 - 489 (9page)

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Introduction: TLR-5, a member of the toll-like receptor (TLR) family, is a element of the type I transmembrane receptors, which are characterized by an intracellular signaling domain homolog to the interleukin-1 receptor. These receptors recognize microbial components, particularly bacterial flagellin. All-trans retinoic acid (atRA, tretinoin), a natural metabolite of vitamin A, acts as a growth and differentiation factor in many tissues, and is also needed for immune functions. In this study, THP-1 human macrophage-monocytes were used to examine the mechanisms by which atRA regulated the expression of TLR-5. Because the molecular mechanism underlying this regulation at the transcriptional level is also unclear, this study examined which putative transcription factors are responsible for TLR-5 expression by atRA in immune cells. Materials and Methods: This study examined whether atRA induces the expression of TLR-5 in THP-1 cells using reverse transcription-polymerase chain reaction (RT-PCR), and which transcription factors are involved in regulating the TLR-5 promoter in RAW264.7 cells using a reporter assay system. Western blot analysis was used to determine which signal pathway is involved in the expression of TLR-5 in atRA-treated THP-1 cells. Results: atRA at a concentration of 10 nM greatly induced the expression of TLR-5 in THP-1 cells. Human TLR-5 promoter contains three Sp-1/GC binding sites around -50 bp and two NF-kB binding sites at -380 bp and -160 bp from the transcriptional start site of the TLR-5 gene. Sp-1/GC is primarily responsible for the constitutive TLR-5 expression, and may also contribute to NF-kB at -160 bp to induce TLR-5 after atRA stimulation in THP-1 cells. The role of NF-kB in TLR-5 expression was further confirmed by inhibitor pyrrolidine dithiocarbamate (PDTC) experiments, which greatly reduced the TLR-5 transcription by 70-80%. Conclusion: atRA induces the expression of the human TLR-5 gene and NF-kB is a critical transcription factor for the atRA-induced expression of TLR-5. Accordingly, it is conceivable that retinoids are required for adequate innate and adaptive immune responses to agents of infectious diseases. atRA and various synthetic retinoids have been used therapeutically in human diseases, such as leukemia and other cancers due to the antiproliferative and apoptosis inducing effects of retinoids. Therefore, understanding the molecular regulatory mechanism of TLR-5 may assist in the design of alternative strategies for the treatment of infectious diseases, leukemia and cancers.
#Tretinoin #Toll-like receptor 5 #Cellular immunity #NF-kappa B

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참고문헌 (26)

참고문헌 신청
Agadir A / 1997 / Retinyl methyl ether down-regulates activator protein 1 transcriptional activation in breast cancer cells / Cancer Res 57 : 3444 ~ 3450 google schola Ballow M / 1993 / Retinoic acid (RA) induced enhancing effects on immunoglobulin (Ig) synthesis of human B-cells / Pediatr Res 33 : 151 ~ google schola Ballow M / 1996 / Modulation of B-cell immunoglobulin synthesis by retinoic acid / Clin Immunol Immunopathol 80 : 73 ~ 81 google schola Ballow M / 1996 / The effects of retinoic acid on immunoglobulin synthesis: role of interleukin 6 / J Clin Immunol 16 : 171 ~ 179 google schola Ballow M / 1997 / Retinoic acid-induced modulation of IL-2mRNA production and IL-2 receptor expression on T Cells / Int Arch Allergy Immunol 113 : 167 ~ 169 google schola

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