Cancer's effect on immunity is studied
One of the potential mechanisms is that B7-H1 creates some sort of physical barrier between tumor cells and the T-cells meant to kill them. This would help explain the selectivity of T-cells against attacking the cancerous cells protected by B7-H1.
However, another hypothesis postulates that the T-cells aren't physically blocked but rather simply deactivated temporarily via some signaling pathway.
A third and rather interesting idea regarding B7-H1's immuno-repressive role is that when B7-H1 interacts with a T-cell, it then starts to transmit cautionary messages to other cancer cells nearby, helping them to become immuno-resistant and to survive an attack by T-cells.
According to Azuma's team, the third postulated mechanism seems to be the most accurate. The group engineered B7-H1 and PD-1 proteins that had impaired signaling abilities and expressed them in cancer cells under experimental conditions.
The team used these proteins to test the mechanism and found that with this impairment, the cancer cells could not relay protective information to other cancer cells, and lysis, or killing of the cancer cells by T-cells as well as anti-cancer drugs, proceeded as expected.
This would seem to suggest that both B7-H1 and PD-1 play their own part in tumors' immune-evasion.
B7-H1 appears to "warn" cancerous cells, promoting the ability to withstand immune responses, and PD-1 appears to have some power to disrupt the normal functioning of T-cells, leading to further immune suppression.
Now, thanks to this line of research, there exists a possible mechanism that scientists and doctors could potentially manipulate in order to better combat cancer.
However, another hypothesis postulates that the T-cells aren't physically blocked but rather simply deactivated temporarily via some signaling pathway.
A third and rather interesting idea regarding B7-H1's immuno-repressive role is that when B7-H1 interacts with a T-cell, it then starts to transmit cautionary messages to other cancer cells nearby, helping them to become immuno-resistant and to survive an attack by T-cells.
According to Azuma's team, the third postulated mechanism seems to be the most accurate. The group engineered B7-H1 and PD-1 proteins that had impaired signaling abilities and expressed them in cancer cells under experimental conditions.
The team used these proteins to test the mechanism and found that with this impairment, the cancer cells could not relay protective information to other cancer cells, and lysis, or killing of the cancer cells by T-cells as well as anti-cancer drugs, proceeded as expected.
This would seem to suggest that both B7-H1 and PD-1 play their own part in tumors' immune-evasion.
B7-H1 appears to "warn" cancerous cells, promoting the ability to withstand immune responses, and PD-1 appears to have some power to disrupt the normal functioning of T-cells, leading to further immune suppression.
Now, thanks to this line of research, there exists a possible mechanism that scientists and doctors could potentially manipulate in order to better combat cancer.
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