Spring Break
Cancer's effect on immunity is studied
Issue date: 4/17/08
Many disease processes involve the manipulation of the immune system. In many cancers, tumor cells are able to evade the immune system, which would ordinarily attack the offending cells, thus prolonging their survival.
The general mechanism for this has been known for a few years. Cancerous cells are able to proffer modified surfaces designed to trick the immune system, the body's defense system, into not attacking the deadly cells.
Research in the laboratory of Takeshi Azuma of the Hopkins School of Medicine looks into this fact as a way to understand the biology of cancers.
The cancerous cells use their modified designs to hide from the immune system as well as to infiltrate, attack, overwhelm and take over the body's healthy cells, leading to the growth and spread of the cancer, unchecked by the body's protective lymphocytes.
The team thinks it has found a molecule that regulates tumors' immune-evasive abilities. This molecule is known as B7-H1. It works as an immune suppressant, bombarding the body's T-cells, immune cells in the lymph system that protect the body from invading cells, with inhibitory messages.
This inhibitition acts as a negative feedback on the immune system, allowing the cancer to continue to grow and spread unchecked.
B7-H1 doesn't just stop the T-cells from working, though; it induces a host of anti-immune behaviors, such as apoptosis, or death of T-cells, the decreased immune response by T-cells and even T-cell exhaustion. These factors all combine to mean that T-cells can't do their job: to protect the body.
The bright side of this dreary story is that T-cells can be turned back on and can resume their auto-protective duties if B7-H1 is turned off, according to new work in Azuma's lab.
However, this on/off ability has several probable causes, and in order to determine through exactly which mechanism the whole process works, the team has studied B7-H1 and its purported receptor PD-1 under several conditions. Their work has led to a better understanding of the mechanism by which the two interact.
The general mechanism for this has been known for a few years. Cancerous cells are able to proffer modified surfaces designed to trick the immune system, the body's defense system, into not attacking the deadly cells.
Research in the laboratory of Takeshi Azuma of the Hopkins School of Medicine looks into this fact as a way to understand the biology of cancers.
The cancerous cells use their modified designs to hide from the immune system as well as to infiltrate, attack, overwhelm and take over the body's healthy cells, leading to the growth and spread of the cancer, unchecked by the body's protective lymphocytes.
The team thinks it has found a molecule that regulates tumors' immune-evasive abilities. This molecule is known as B7-H1. It works as an immune suppressant, bombarding the body's T-cells, immune cells in the lymph system that protect the body from invading cells, with inhibitory messages.
This inhibitition acts as a negative feedback on the immune system, allowing the cancer to continue to grow and spread unchecked.
B7-H1 doesn't just stop the T-cells from working, though; it induces a host of anti-immune behaviors, such as apoptosis, or death of T-cells, the decreased immune response by T-cells and even T-cell exhaustion. These factors all combine to mean that T-cells can't do their job: to protect the body.
The bright side of this dreary story is that T-cells can be turned back on and can resume their auto-protective duties if B7-H1 is turned off, according to new work in Azuma's lab.
However, this on/off ability has several probable causes, and in order to determine through exactly which mechanism the whole process works, the team has studied B7-H1 and its purported receptor PD-1 under several conditions. Their work has led to a better understanding of the mechanism by which the two interact.
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