level 11
![[勉强]](/static/emoticons/u52c9u5f3a.png)
level 14
Toll-like receptor 4 (TLR4) (a) and TLR9 (b) signaling. TLR4 signaling activates two pathways originating at the intracytoplasmic domain of TLR4. One is the MyD88-dependent pathway, which sequentially activates NF-κB and MAPK cascades (not shown) through IRAK and TRAF6. This pathway is crucial for cytokine production. The other is the MyD88-independent pathway, which can lead to activation of NF-κB and MAPK cascades with delayed kinetics.Kaisho, Tsuneyasu, and Shizuo Akira. "Dendritic-cell function in Toll-like receptor-and MyD88-knockout mice." Trends in immunology 22.2 (2001): 78-83.
然而并没有解释我的问题啊
2015年11月12日 16点11分
level 13
![[酷]](/static/emoticons/u9177.png)
level 8
![[阴险]](/static/emoticons/u9634u9669.png)
level 7
level 7
第一段说的是，和TLR4有关。TLR4变异会导致疗效变差。
第二段说的是，MYD88透过TLR影响疗效。
两段唯一共同的是谈TLR的影响，不是一回事。
2015年11月13日 14点11分
11
第二段说的是，MYD88透过TLR影响疗效。
两段唯一共同的是谈TLR的影响，不是一回事。
level 11
驭龙氏
楼主
Back to Coley: a 21st century perspective.
We now realize that Coley’s mixed
toxins must have been powerful stimulants
of TLRs140, inducing a range of inflammatory
mediators, not just TNF. The closest recent
approximation to Coley’s work is probably
the successful local treatment of bladder
cancer with bacillus Calmette–Guerin141.
Current thinking is that both bacillus
Calmette–Guerin and Coley’s toxins trigger
a desirable inflammatory response, through
TLRs, that not only stimulates macrophages
to kill tumour cells but also promotes the
development of sustained and effective adaptive
immunity to the tumour142. This type of
response may also contribute to successful
Back to Coley: a 21st century perspective.
We now realize that Coley’s mixed
toxins must have been powerful stimulants
of TLRs140, inducing a range of inflammatory
mediators, not just TNF. The closest recent
approximation to Coley’s work is probably
the successful local treatment of bladder
cancer with bacillus Calmette–Guerin141.
Current thinking is that both bacillus
Calmette–Guerin and Coley’s toxins trigger
a desirable inflammatory response, through
TLRs, that not only stimulates macrophages
to kill tumour cells but also promotes the
development of sustained and effective adaptive
immunity to the tumour142. This type of
response may also contribute to successful
2015年11月17日 08点11分
13
We now realize that Coley’s mixed
toxins must have been powerful stimulants
of TLRs140, inducing a range of inflammatory
mediators, not just TNF. The closest recent
approximation to Coley’s work is probably
the successful local treatment of bladder
cancer with bacillus Calmette–Guerin141.
Current thinking is that both bacillus
Calmette–Guerin and Coley’s toxins trigger
a desirable inflammatory response, through
TLRs, that not only stimulates macrophages
to kill tumour cells but also promotes the
development of sustained and effective adaptive
immunity to the tumour142. This type of
response may also contribute to successful
Back to Coley: a 21st century perspective.
We now realize that Coley’s mixed
toxins must have been powerful stimulants
of TLRs140, inducing a range of inflammatory
mediators, not just TNF. The closest recent
approximation to Coley’s work is probably
the successful local treatment of bladder
cancer with bacillus Calmette–Guerin141.
Current thinking is that both bacillus
Calmette–Guerin and Coley’s toxins trigger
a desirable inflammatory response, through
TLRs, that not only stimulates macrophages
to kill tumour cells but also promotes the
development of sustained and effective adaptive
immunity to the tumour142. This type of
response may also contribute to successful
渣排版全赖nature review的editor
2015年11月17日 08点11分
level 7
为何这事容易让人迷惑？因为事情有点像注射疫苗。
适当的疫苗可以激发抗体。
适当的发炎可以激发抗癌。
如果疫苗强度减弱不足，可能致病。
同理，发炎会致癌。
完全切断发炎机制呢？as might be expected,....抗癌了
前面两行就让楼主感觉矛盾了。关键在发炎的强度，类似疫苗的强度。
2015年11月17日 10点11分
14
适当的疫苗可以激发抗体。
适当的发炎可以激发抗癌。
如果疫苗强度减弱不足，可能致病。
同理，发炎会致癌。
完全切断发炎机制呢？as might be expected,....抗癌了
前面两行就让楼主感觉矛盾了。关键在发炎的强度，类似疫苗的强度。
主要是那个as expected我搞不懂这逻辑，说免疫系统有抑癌和促癌两面性可以理解，但是先说免疫系统抑癌，果然新发现表明免疫系统被干掉之后癌细胞长得不好了，这个逻辑接受不了……
2015年11月17日 11点11分
