已入深夜,您辛苦了!由于当前在线用户较少,发布求助请尽量完整地填写文献信息,科研通机器人24小时在线,伴您度过漫漫科研夜!祝你早点完成任务,早点休息,好梦!

CD40-mediated up-regulation of Toll-like receptor 4-MD2 complex on the surface of murine dendritic cells

作者
Davor Frleta,Randolph J. Noelle,William F. Wade
出处
期刊:Journal of Leukocyte Biology [Oxford University Press]
卷期号:74 (6): 1064-1073 被引量:16
标识
DOI:10.1189/jlb.0203062
摘要

Toll-like receptors (TLRs) recognize pathogen-associated molecular patterns, which are non-self macromolecular components of pathogens that allow the innate-immune system to recognize infection. TLRs are expressed on macrophages and dendritic cells (DC). TLR stimulation or CD40 agonists can induce inflammatory cytokine secretion from macrophages and DC, and promote DC maturation. The regulation of TLR expression by inflammation has begun to be explored. Our studies have focused on the regulation of TLR4 surface expression on DC. TLR4, along with the adaptor molecule MD2, is involved in the recognition of lipopolysaccharide (LPS). CD40 stimulation via cross-linked anti-CD40 monoclonal antibody (mAb) up-regulates TLR4-MD2 surface expression on a DC cell line (DC2.4) and on ex vivo-cultured splenic DC. LPS treatment down-regulated surface TLR4-MD2 on DC2.4 cells, but if combined with anti-CD40 mAb, increased TLR4-MD2 expression was observed. The increased TLR4-MD2 surface expression by any treatment did not correlate with TLR4 mRNA levels. The functional consequence of increased TLR4-MD2 expression following LPS and anti-CD40 treatment was examined. Although CD40 prestimulation did slightly enhance interleukin-12p70 secretion after LPS restimulation, simultaneous anti-CD40 mAb and LPS treatment, which up-regulates TLR4-MD2 complex, does not restore DC responsiveness to subsequent LPS.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
刚刚
JamesPei应助热闹的冬天采纳,获得10
2秒前
2秒前
大雪纷飞发布了新的文献求助10
2秒前
3秒前
SciGPT应助热闹的冬天采纳,获得10
3秒前
爆米花应助热闹的冬天采纳,获得10
3秒前
我是老大应助157采纳,获得10
4秒前
4秒前
5秒前
所所应助吴志亮采纳,获得10
5秒前
6秒前
niuniu完成签到,获得积分10
7秒前
8秒前
研友_08okB8完成签到,获得积分10
8秒前
郜伯云完成签到,获得积分10
9秒前
大力可燕完成签到,获得积分10
9秒前
wz发布了新的文献求助10
10秒前
情怀应助li采纳,获得10
10秒前
上岸吧发布了新的文献求助10
11秒前
Cu完成签到,获得积分10
11秒前
woshi123应助582843216采纳,获得10
12秒前
研友_08okB8发布了新的文献求助10
12秒前
美味的屑狐狸完成签到 ,获得积分10
12秒前
13秒前
郜伯云发布了新的文献求助10
13秒前
张欢馨应助樱桃小贩采纳,获得10
14秒前
coechor完成签到,获得积分10
15秒前
快乐小兰发布了新的文献求助10
15秒前
lll发布了新的文献求助10
15秒前
16秒前
17秒前
oi发布了新的文献求助10
17秒前
17秒前
心态好应助无私的元霜采纳,获得10
18秒前
吴志亮发布了新的文献求助10
19秒前
wz完成签到,获得积分10
20秒前
21秒前
JamesPei应助每天100次采纳,获得20
21秒前
态度发布了新的文献求助10
22秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Reducing Compassion Fatigue, Secondary Traumatic Stress and Burnout 600
China Pluperfect I: Epistemology of Past and Outside in Chinese Art 520
Matrix Methods in Data Mining and Pattern Recognition Second Edition 510
Mammalian Synthetic Biology 500
Auslegungsgeschichte 500
Cosmos as Art Object: Studies in Plato's Timaeus and Other Dialogues 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7639270
求助须知:如何正确求助?哪些是违规求助? 9212354
关于积分的说明 19761936
捐赠科研通 7205941
什么是DOI,文献DOI怎么找? 3275996
关于科研通互助平台的介绍 2437546
邀请新用户注册赠送积分活动 2273227