英國癌症研究院的科學家發現了一種他們稱之為"危險受體"的細胞,這種細胞也許能刺激人體免疫系統對癌細胞作出反應。
人活著的時候,體內的細胞總是在不斷的死亡,同時又不斷生出新的細胞來接替死去的。
有時候,比如受了傷的時候,細胞就會產生非正常的死亡。
科學家在對一組叫作"受體"的人體細胞進行研究時發現,當這種細胞受刺激後,它們會向大腦發出信號,而大腦會隨即作出反應。
"危險受體"
這一研究確認,受體細胞能夠阻止非正常的細胞死亡。所以研究人員把這種細胞叫作"危險受體"。
領導這一研究的索薩博士說,科學家已經知道,諸如細菌和病毒這樣的污染性有機體,能直接觸發人體免疫系統的反應。
索薩博士說,如果研究發現受傷信號也能刺激免疫系統的話,也許能讓科學家在治療癌症的疫苗和療法方面找到新的路子。
事實上癌症也是可能觸發免疫系統的反應的,因為惡性腫瘤中經常有非正常死亡的集束細胞。
科學家認為,對"危險受體"這種細胞有了更多瞭解後, 也許能夠在利用人體免疫系統對抗自身癌症的研究方面有 很大幫助。
Cancer 'danger receptor' found
Dendritic cells alert the rest of the immune system to an invader |
A "danger receptor" that may kick-start an immune reaction to cancer in the body has been found by UK researchers.
It picks up signs of cell death caused by injury or tumours and mobilises the body's defences, Nature reports.
The finding may explain why some tumour-killing drugs partly work by setting off an immune response.
Better understanding of the receptor could help develop cancer treatments that harness the immune system, the London Research Institute team said.
Cell death is a normal process in the body which keeps growth and repair ticking over and keeps tissue healthy.
After a 15-year hunt, we've identified the first 'danger receptor' - one which senses abnormal cell death and then triggers an immune response Dr Caetano Reis e Sousa, study leader |
But sometimes there is an abnormal type of cell death called necrosis.
It has been thought for many years that the body somehow senses this abnormal cell death and sets off an immune reaction.
From an evolutionary point of view this would make sense as injury puts the body at risk of infection and an immune response would be a sensible precaution.
However, until now no receptor capable of detecting this abnormal cell death had been found.
The researchers discovered that the DNGR-1 receptor on a type of immune cell called a dendritic cell mobilises an immune response after coming across this abnormal cell death.
Dendritic cells act as messengers, alerting other types of immune cells to kill invaders, such as viruses and bacteria.
Trigger
The researchers said tumours could also trigger this type of immune reaction because they often contain clusters of cells undergoing this type of cell death as they have a limited blood supply.
Dr Caetano Reis e Sousa, lead author based at Cancer Research UK's London Research Institute, said: "After a 15-year hunt, we've identified the first 'danger receptor' - one which senses abnormal cell death and then triggers an immune response.
"The detection of 'danger' could explain some situations when a tumour triggers an immune reaction against itself."
He said manipulating this system could be beneficial in treating cancer but also in other areas, such as preventing rejection in organ transplantation.
"There is a theory that some cancer-killing drugs kill tumour cells in such a way that triggers the immune system against them so they have a double whammy."
Dr Lesley Walker, director of information at Cancer Research UK, said: "The concept of using the body's immune system to fight cancer has been around for decades, but advances in recent years have made this field of research a very exciting one.
"The results of this study are really important scientifically and a step towards understanding how to manipulate the immune system to treat cancer in the future."
Key Jigsaw Piece in Cancer Discovered
Tuesday 6 January
Scientists have discovered a crucial piece in the cancer jigsaw, identifying one key enzyme responsible for allowing cancer to spread, according to a study published in Cancer Cell.
Cancer metastasis, the spreading of cancer from its original location, is responsible for 90 per cent of cancer related deaths.
Lead researcher Dr Janine Erler from The Institute of Cancer Research has discovered that the LOX enzyme is crucial in promoting metastasis and says:
“This research has identified how to prevent a cancer from establishing itself in a new area of the body. This is the crucial missing piece in the jigsaw that scientists have been searching for and is the first time one key enzyme has been identified as being responsible for effectively allowing the cancer to spread.
“LOX works by sending out signals to prepare a new area of the body for the cancer to set up camp. Without this preparation process the new environment would be too hostile for the cancer to grow. If we can interrupt the body’s ability to prepare new locations for the cancer to spread to, we can effectively prevent cancer metastasis.”
The paper looked specifically at how LOX enables the spread of breast cancer, but researchers have evidence that the enzyme is also crucial in the metastasis of other common cancers.
The Institute of Cancer Research hopes to use the discovery of how LOX works to aid the spread of cancer to develop new drug treatments to prevent cancer metastasis.
“Cancer metastasis is very difficult to treat and this new discovery provides real hope that we can develop a drug which will fight the spreading of cancer,” Dr Erler said.
Ends
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