Release date: 2017-06-21
Recently, a study published in Cell magazine entitled "Interferon-γ Drives Treg Fragility to Promote Anti-tumor Immunity" confirmed that targeting regulatory T cells (Tregs) is expected to be an effective way to treat cancer. At the same time, research reveals an important mechanism of cancer immunotherapy, which is expected to further expand the potential of immunotherapeutics to enable it to treat more cancers.
As a type of T cell, Tregs can help maintain a delicate balance of the body's immune system. Professor Dario Vignali, the author of the study, said: "The cells can detect and eliminate the threat of the body and prevent our own cells from being harmed. However, in cancer, Tregs may be harmful. Through immunosuppression, They prevent the immune system from detecting and killing cancer cells."
Although the development of drugs to clear Tregs appears to be a logical anticancer therapy, this anticancer pathway may lead to life-threatening autoimmune complications. Therefore, scientists need to find ways to selectively target Tregs in tumors.
3-D microscopic image of a tumor showing Tregs (green), blood vessels (red) and tumor matrix (blue) (Source: Vignali Lab)
Key gene
A few years ago, Professor Vignali and his colleagues found that a surface protein called neuropilin-1 (Nrp1) was expressed on almost all Tregs infiltrating into mouse tumors. In the harsh tumor microenvironment, Nrp1 is important for maintaining the function, integrity and survival of Tregs. Therefore, Nrp1 helps to suppress the body's natural anti-tumor immune response, thereby helping the tumor to survive.
The researchers are pleased that blocking or deleting Nrp1 on Tregs in mice only affects their function in the tumor and does not affect other parts of the body. Therefore, it does not induce autoimmunity while destroying the tumor. Or an inflammatory disease.
In this latest study, scientists have found an interesting finding: in mice, when Tregs lose Nrp1, they not only lose their immunosuppressive effects, but also become active "participants" of anti-tumor immune responses. More importantly, the study also found that the level of Treg subpopulation expressing Nrp1 was much higher in cancer patients with poor prognosis. This suggests that the results of the study in mice may also apply to humans.
Specifically, the research team constructed a transgenic mouse model. In this model, half of the Trp cell population's Nrp1 gene was deleted. As a result, it was found that tumor growth of such treated mice was significantly reduced as compared with normal mice in which all of the Tregs were present in Nrp1.
Abigail E. Overacre-Delgoffe, the lead author of the study, said: "The removal of Nrp1's Tregs not only reduces the ability of the immune system to detect and kill cancer cells, but also prevents normal Treg cell populations from exerting their immunosuppressive functions. This allows the immune system to see and attack the tumor."
Amazing discovery
In addition, genomic and cellular analysis revealed that the immune molecule IFN-γ affected the function of Tregs in mice, especially Tregs in the tumor microenvironment.
Using another transgenic mouse model, the team found that the role of IFNγ in attenuating Tregs function is critical to the success of immunotherapy targeting PD-1.
Professor Vignali said: "Although we believe that IFN-γ may affect the function of Tregs and thus affect the outcome of immunotherapy, the 'importance' of this effect surprised us. When we removed IFN-γ from Tregs At the time of receptors (so that they are no longer sensitive to the effects of IFNγ), immunotherapeutics are completely ineffective. In essence, IFN-γ appears to make Tregs "fragile", thereby causing them to lose immunosuppression. Function. Therefore, making Tregs "fragile" may be the key to effective cancer immunotherapy."
Significant
The authors believe that this finding is significant. Because, the study suggests that if a subset of tumor-associated Tregs are obtained, losing their immunosuppressive function (perhaps using IFN-γ to achieve this), it may be sufficient to trigger a chain reaction. These Tregs, which lose immunosuppressive function, will affect other tumor-associated Tregs, thereby promoting an anti-tumor immune response without producing autoimmune side effects. In addition, tracking the "fragility" of Tregs may be an effective way to monitor whether immunotherapy works.
Other related
Regarding how important IFN-γ is to cancer immunotherapy, Xiaobian once confirmed in Nature! To make a better cancer immunotherapy, this molecule is very important. There is a summary in this article, which involves 1 Nature, 1 Cell and 1 NEJM. Among them, the Nature paper reveals the mechanism by which IFN-γ exerts an anti-tumor effect: targeting vascular cells and cutting off the blood supply to the tumor. Two other papers have revealed the association of IFN-γ with immunotherapeutic resistance.
Source: Bio-Exploration (micro-signal biodiscover)
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