人體可以精確記錄回憶很久以前遇到的病毒及細(xì)菌,，使我們不會(huì)經(jīng)歷二次麻疹和水痘,，這也是疫苗發(fā)揮功效的原因。
但研究人員對(duì)于記憶系統(tǒng)的機(jī)制仍不是很清楚,。一個(gè)國(guó)際合作小組發(fā)現(xiàn)一條重要線索,，可解釋免疫系統(tǒng)如何記憶曾經(jīng)遇到過(guò)的敵人，并且快速地作出反應(yīng),。研究結(jié)果刊載于10月23日的PNAS中,。
Wisconsin-Madison大學(xué)的研究人員Marulasiddappa Suresh帶領(lǐng)的研究小組鑒定出一種與刺激免疫細(xì)胞活化過(guò)程有關(guān)的蛋白質(zhì)。
免疫系統(tǒng)T細(xì)胞能夠攻擊病毒感染的細(xì)胞,、外源細(xì)胞和癌細(xì)胞,，并且在細(xì)胞表面傳感器抗原受體的刺激下產(chǎn)生記憶。這種被研究人員稱為L(zhǎng)ck的蛋白,，在T細(xì)胞對(duì)病原體特征進(jìn)行記憶的過(guò)程中發(fā)揮至關(guān)重要的作用,。Lck可以幫助未曾暴露于特異抗原的原始T細(xì)胞（naïve T cells）捕獲、收藏入侵抗原以備后患,。感染或者接種疫苗后,，Lck啟動(dòng)一條生化途徑,，擴(kuò)大了發(fā)揮抵抗作用的T細(xì)胞數(shù)量,。
等到感染被鎮(zhèn)壓后,，抵抗此抗原的T細(xì)胞大軍數(shù)量急劇下降,。但有一小部分保留下來(lái)，即所謂的記憶細(xì)胞,，保留了侵略者的印記,，在若干年后相同的病原體卷土重來(lái)時(shí)，記憶細(xì)胞能夠迅速作出反應(yīng),。
Suresh等人發(fā)現(xiàn),，與原始T細(xì)胞不同，記憶T細(xì)胞的活動(dòng)范圍不止于淋巴系統(tǒng),，它周游身體各處,，輔助身體感覺(jué)、更加迅速消滅先前遇到過(guò)的抗原,。這項(xiàng)新發(fā)現(xiàn)不也可以輔助抗AIDS等病毒的疫苗開(kāi)發(fā),，為自體免疫疾病患者和器官排斥反應(yīng)的患者帶來(lái)福音,。
英文原文：
Scientists find key to immune system’s ability to remember
Its ability to accurately catalog and recall long-past encounters with viruses, bacteria and other pathogens is why we get the measles or chicken pox only once, and is why exposure to deactivated virus particles in vaccines confers protection from disease.
But how that memory system works — how it acts at the finest level of detail to thwart the pathogens that invade our bodies — is not well understood. Now, however, an international team of scientists has ferreted out an important clue to how the key cells of the immune system are able to remember old foes and quickly mount a response to hold them at bay.
Writing this week (Oct. 23) in the Proceedings of the National Academy of Sciences (PNAS), a team of researchers led by University of Wisconsin-Madison researcher Marulasiddappa Suresh identify the role of a protein that is important in stimulating the cells of the immune system, whose role is to take quick and effective action when agents of disease reinvade the body.
"We have found at least a part of how the immune system remembers its encounters," says Suresh, a professor of pathobiological sciences in the UW-Madison School of Veterinary Medicine. "We now know one of the reasons why we get such a quick (immune) response" when we are exposed to pathogens we've experienced before.
The new insight is important not only because it sheds light on the biochemical intricacies of immune system memory, but also because it may one day aid in the development of vaccines against infections such as AIDS, and help victims of autoimmune diseases and transplant patients whose immune systems reject donor organs.
The protein, which scientists call Lck, is essential for immune system T cells — white blood cells that attack virus-infected cells, foreign cells and cancer cells — to cement the memory induced by cell surface sensors known as antigen receptors that act to identify the signatures of pathogens like measles virus and HIV, agents that hide inside cells.
Lck is important in helping "naïve" T cells — those cells that have never been exposed to a particular pathogen — capture the receptor template of the invading agent and store it for future reference. Among the millions of naïve T cells, there are a few that are primed for active duty against an individual infectious agent. Following infection or vaccination, Lck initiates a biochemical chain of events that vastly increases the number of T cells that march off to combat the invader.
After the infection subsides, the number of T cells marshaled to fight that agent decreases dramatically. But a smaller subset, known as "memory" cells, retains the imprint of its previous encounter should the pathogen make a return appearance.
According to the study, while Lck primes naïve cells to fight a pathogen, it is not required by memory cells, which initiate the fast and furious response when that same pathogen comes calling again years later. Unlike naïve T cells, which are confined to the lymphatic system, memory T cells are found everywhere in the body, enabling them to sense and react more quickly when an infectious agent is reencountered.
"Now we know one of the reasons we get such a quick response and clearance (of the pathogen) with re-infection," Suresh explains. "If you increase the size of your army, you can clear your enemies faster. The memory T cells are greater in number and they are more potent."
The new insight could help refine therapeutic targets to treat autoimmune diseases and may inform new strategies for suppressing T cell response after transplantation. Now, transplant patients require lifelong regimens of drugs to suppress immune response to the foreign cells in the donated organ.
In addition to Suresh, authors of the new PNAS report include Kavita Tewari, Jane Walent and John Svaren, all of UW-Madison, and Rose Zamoyska of the United Kingdom's Medical Research Council National Institute for Medical Research. The research was funded by the U.S. Public Health Service.
