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Production of $TGF-{eta}1$ as a Mechanism for Defective Antigen-presenting Cell Function of Macrophages Generated in vitro with M-CSF
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  • Production of $TGF-{eta}1$ as a Mechanism for Defective Antigen-presenting Cell Function of Macrophages Generated in vitro with M-CSF
  • Production of $TGF-{eta}1$ as a Mechanism for Defective Antigen-presenting Cell Function of Macrophages Generated in vitro with M-CSF
저자명
Lee. Jae-Kwon,Lee. Young-Ran,Lee. Young-Hee,Kim. Kyung-Jae,Lee. Chong-Kil
간행물명
Immune network : official journal of the Korean association of immunobiologists
권/호정보
2009년|9권 1호|pp.27-33 (7 pages)
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

Macrophages generated in vitro using macrophage-colony stimulating factor (M-CSF) and interleukin (IL)-6 from bone marrow cells (BM-Mp) are defective in antigen presenting cell (APC) function as shown by their ability to induce the proliferation of anti-CD3 mAb-primed syngeneic T cells. However, they do express major histocompatibility (MHC) class I and II molecules. accessory molecules and intracellular adhesion molecules. Here we demonstrate that the defective APC function of macrophages is mainly due to production of $TGF-{eta}1$ by BM-Mp. Methods: Microarray analysis showed that $TGF-{eta}1$ was highly expressed in BM-Mp, compared to a macrophage cell line, B6D. which exerted efficient APC function. Production of $TGF-{eta}1$ by BM-Mp was confirmed by neutralization experiments of $TGF-{eta}1$ as well as by real time-polymerase chain reaction (PCR). Results: Addition of $anti-TGF-{eta}1$ monoclonal antibody to cultures of BM-Mp and anti-CD3 mAb-primed syngeneic T cells efficiently induced the proliferation of syngeneic T cells. Conversely, the APC function of B6D cells was almost completely suppressed by addition of $TGF-{eta}1$. Quantitative real time-PCR analysis also confirmed the enhanced expression of $TGF-{eta}1$ in BM-Mp. Conclusion: The defective APC function of macrophages generated in vitro with M-CSF and IL-6 was mainly due to the production of $TGF-{eta}1$ by macrophages.