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Monash University
A study published in Leukemia has revealed a mechanism by which chronic lymphocytic leukemia (CLL) evades the immune system.
“It turns out that cancer cells are very good at sabotaging the immune system, using various tricks that confuse immune cells and ‘smoke screens’ preventing immune cells from recognizing the cancer,” said study author Fabienne Mackay, PhD, of Monash University in Melbourne, Victoria, Australia.
She and her colleagues believe they have determined exactly how CLL confuses the immune system and devised a way to stop it without destroying the patient’s immune system.
The team noted that B cells rely on the protein BAFF to survive. And each B cell has 3 different kinds of receptors that detect the presence of BAFF in the blood—TACI, BAFF-R, and BCMA.
The researchers discovered that, in CLL patients, the TACI receptors of cancerous B cells over-produce interleukin-10 (IL-10), which tricks the immune system into thinking nothing is wrong, allowing CLL to thrive undetected.
“We found that, when the receptor called TACI was blocked, it prevented the secretion of IL-10 without eliminating normal B cells,” Dr Mackay said. “Without IL-10, the tumor can no longer keep the immune system at bay, which means the patient’s immune system can be ‘kick-started’ again to fight infections and cancers.”
“This is very exciting because it means that B cells stay alive and well to do their job in the immune system fighting other infections. It also means the over-production of IL-10 is stopped, and the CLL cells are now exposed to immune cells specialized in fighting cancers.”
Dr Mackay said her team’s discovery may be relevant for cancers other than CLL and could change the way they are treated.
“The best weapon we have for fighting cancer is the immune system itself,” Dr Mackay noted. “It can sense the presence of an infection but also the emergence of a cancer.”
Photo courtesy of
Monash University
A study published in Leukemia has revealed a mechanism by which chronic lymphocytic leukemia (CLL) evades the immune system.
“It turns out that cancer cells are very good at sabotaging the immune system, using various tricks that confuse immune cells and ‘smoke screens’ preventing immune cells from recognizing the cancer,” said study author Fabienne Mackay, PhD, of Monash University in Melbourne, Victoria, Australia.
She and her colleagues believe they have determined exactly how CLL confuses the immune system and devised a way to stop it without destroying the patient’s immune system.
The team noted that B cells rely on the protein BAFF to survive. And each B cell has 3 different kinds of receptors that detect the presence of BAFF in the blood—TACI, BAFF-R, and BCMA.
The researchers discovered that, in CLL patients, the TACI receptors of cancerous B cells over-produce interleukin-10 (IL-10), which tricks the immune system into thinking nothing is wrong, allowing CLL to thrive undetected.
“We found that, when the receptor called TACI was blocked, it prevented the secretion of IL-10 without eliminating normal B cells,” Dr Mackay said. “Without IL-10, the tumor can no longer keep the immune system at bay, which means the patient’s immune system can be ‘kick-started’ again to fight infections and cancers.”
“This is very exciting because it means that B cells stay alive and well to do their job in the immune system fighting other infections. It also means the over-production of IL-10 is stopped, and the CLL cells are now exposed to immune cells specialized in fighting cancers.”
Dr Mackay said her team’s discovery may be relevant for cancers other than CLL and could change the way they are treated.
“The best weapon we have for fighting cancer is the immune system itself,” Dr Mackay noted. “It can sense the presence of an infection but also the emergence of a cancer.”
Photo courtesy of
Monash University
A study published in Leukemia has revealed a mechanism by which chronic lymphocytic leukemia (CLL) evades the immune system.
“It turns out that cancer cells are very good at sabotaging the immune system, using various tricks that confuse immune cells and ‘smoke screens’ preventing immune cells from recognizing the cancer,” said study author Fabienne Mackay, PhD, of Monash University in Melbourne, Victoria, Australia.
She and her colleagues believe they have determined exactly how CLL confuses the immune system and devised a way to stop it without destroying the patient’s immune system.
The team noted that B cells rely on the protein BAFF to survive. And each B cell has 3 different kinds of receptors that detect the presence of BAFF in the blood—TACI, BAFF-R, and BCMA.
The researchers discovered that, in CLL patients, the TACI receptors of cancerous B cells over-produce interleukin-10 (IL-10), which tricks the immune system into thinking nothing is wrong, allowing CLL to thrive undetected.
“We found that, when the receptor called TACI was blocked, it prevented the secretion of IL-10 without eliminating normal B cells,” Dr Mackay said. “Without IL-10, the tumor can no longer keep the immune system at bay, which means the patient’s immune system can be ‘kick-started’ again to fight infections and cancers.”
“This is very exciting because it means that B cells stay alive and well to do their job in the immune system fighting other infections. It also means the over-production of IL-10 is stopped, and the CLL cells are now exposed to immune cells specialized in fighting cancers.”
Dr Mackay said her team’s discovery may be relevant for cancers other than CLL and could change the way they are treated.
“The best weapon we have for fighting cancer is the immune system itself,” Dr Mackay noted. “It can sense the presence of an infection but also the emergence of a cancer.”