Thin, active invisibility cloak demonstrated for first time

Nov. 12, 2013 — Invisibility cloaking is no longer the stuff of science fiction: two researchers in The Edward S. Rogers Sr. Department of Electrical & Computer Engineering have demonstrated an effective invisibility cloak that is thin, scalable and adaptive to different types and sizes of objects.

Professor George Eleftheriades and PhD student Michael Selvanayagam have designed and tested a new approach to cloaking -- by surrounding an object with small antennas that collectively radiate an electromagnetic field. The radiated field cancels out any waves scattering off the cloaked object. Their paper 'Experimental demonstration of active electromagnetic cloaking' appears today in the journal Physical Review X.

"We've taken an electrical engineering approach, but that's what we are excited about," says Eleftheriades. "It's very practical."

Picture a mailbox sitting on the street. When light hits the mailbox and bounces back into your eyes, you see the mailbox. When radio waves hit the mailbox and bounce back to your radar detector, you detect the mailbox. Eleftheriades and Selvanyagam's system wraps the mailbox in a layer of tiny antennas that radiate a field away from the box, cancelling out any waves that would bounce back. In this way, the mailbox becomes undetectable to radar.

"We've demonstrated a different way of doing it," says Eleftheriades. "It's very simple: instead of surrounding what you're trying to cloak with a thick metamaterial shell, we surround it with one layer of tiny antennas, and this layer radiates back a field that cancels the reflections from the object."

Their experimental demonstration effectively cloaked a metal cylinder from radio waves using one layer of loop antennas. The system can be scaled up to cloak larger objects using more loops, and Eleftheriades says the loops could become printed and flat, like a blanket or skin. Currently the antenna loops must be manually attuned to the electromagnetic frequency they need to cancel, but in future they could function both as sensors and active antennas, adjusting to different waves in real time, much like the technology behind noise-cancelling headphones.

Work on developing a functional invisibility cloak began around 2006, but early systems were necessarily large and clunky -- if you wanted to cloak a car, for example, in practice you would have to completely envelop the vehicle in many layers of metamaterials in order to effectively "shield" it from electromagnetic radiation. The sheer size and inflexibility of the approach makes it impractical for real-world uses. Earlier attempts to make thin cloaks were not adaptive and active, and could work only for specific small objects.

Beyond obvious applications, such as hiding military vehicles or conducting surveillance operations, this cloaking technology could eliminate obstacles -- for example, structures interrupting signals from cellular base stations could be cloaked to allow signals to pass by freely. The system can also alter the signature of a cloaked object, making it appear bigger, smaller, or even shifting it in space. And though their tests showed the cloaking system works with radio waves, re-tuning it to work with Terahertz (T-rays) or light waves could use the same principle as the necessary antenna technology matures.

"There are more applications for radio than for light," says Eleftheriades. "It's just a matter of technology -- you can use the same principle for light, and the corresponding antenna technology is a very hot area of research."

View the original article here

AstraZeneca CEO gets two cheers after first year in job

By Ben Hirschler

LONDON (Reuters) - Fixing ailing drugmaker AstraZeneca remains a work in progress for Chief Executive Pascal Soriot, with sales and profits still heading firmly downhill after his first year in the job.

Yet confidence is slowly building that he may have the right long-term prescription for the British group, helped by some lessons learnt at his past employer Roche.

Soriot has shunned a big acquisition as a way to plug the deep revenue gap left by multiple patent expiries, opting instead for a string of smaller deals, a reboot of the drug pipeline and a shake-out of top management.

His goal of "achieving scientific leadership" may fall short on the kind of hard financial targets that some investors would like, but it has resonated with many younger researchers who felt the group was drifting, following past R&D setbacks. It has already accelerated work on several promising cancer drugs.

"When I talk to people in the industry about AstraZeneca, it is a place where people now want to go and work - and that hasn't been true for about 10 or 15 years," said Dan Mahony, a fund manager at Polar Capital, who has raised his stake in the company in the past year.

Reversing AstraZeneca's poor record in drug research is Soriot's top priority, so staff morale matters. Rival executives say he is borrowing some ideas from Switzerland's Roche.

Roche - particularly its Genentech biotech unit, which Soriot used to head - is renowned for its R&D successes, something Soriot hopes to replicate with a $500 million move of AstraZeneca operations to Cambridge, a British science hub.

"I see him implementing some of the same strategies that have been adopted by Roche, in terms of focusing on highly innovative products and taking risks," said one senior Roche insider.

"You have to have patience when your company is going through these kinds of adjustments."

Soriot told Reuters in June that turning around the company would take three to four years.

Industry analysts predict sales and earnings will continue to fall to 2017 or beyond, since a big hit is still to come when top-selling cholesterol fighter Crestor loses patent cover in 2016.

AstraZeneca's problems are not unique, but its patent expiries are bigger and longer-lasting than at rivals such as British peer GlaxoSmithKline. Its pure focus on prescription drugs also means it lacks the buffer of consumer-focused sales seen at the likes of GSK and Switzerland's Novartis.

SELECTED BETS

Things could be different with a large acquisition that might bring in new revenue overnight - a strategy adopted by some other drugmakers, such as Pfizer, faced with similar sales cliffs. Soriot, however, says such a deal is unlikely, though he hasn't ruled it out altogether.

Since taking over on October 1, 2012, the one-time French veterinary surgeon has spent a modest $2 billion on buying companies like heart drug firm Omthera, respiratory medicine specialist Pearl and Amplimmune in oncology.

That is far below the $20 billion analysts believe he could afford, and the cautious approach is cheered by shareholders who worry about the risk of wasting cash on over-priced deals.

"He is focusing on the appropriate areas like bolt-on rather than major acquisitions, restructuring management and shifting R&D to Cambridge," one of AstraZeneca's 30 largest shareholders said, speaking on condition of anonymity.

Proving the value of this strategy will take time, however.

"The M&A has looked okay, but it is still too early to say if it is really going to shore up the pipeline," a second leading investor said.

In the meantime, Soriot also has his work cut out trying to bolster AstraZeneca's existing drugs business, where he has raised investment in new heart drug Brilinta, in the hope of a pick-up in sales towards the end of this year.

Investors, though, are not banking on a quick turnaround for either Brilinta or the company's important diabetes business.

Emerging markets, another key growth driver, are also a challenge as economies slow and China becomes a far more difficult market following an anti-corruption drive that has disrupted drug sales.

China is an especially important market for AstraZeneca, representing some 7 percent of the group's total revenue.

Given its well-known problems, investor expectations for AstraZeneca are the lowest among all major drugmakers, with the shares trading at just 10 times this year's expected earnings, against more than 16 times for Roche.

But they do offer a chunky 5.5 percent dividend yield as a consolation for those investors who are betting such "broken" drug stocks have a way of mending themselves, as Bernstein analyst Tim Anderson says has often been the case in history.

"I'm patient," said Polar Capital's Mahony. "It might take three years, but I'll get paid the best part of 6 percent in a dividend while I'm waiting."

(Additional reporting by Sinead Cruise; Editing by Will Waterman)

View the original article here

First step to reduce plant need for nitrogen fertilizer uncovered

Sep. 27, 2013 — Nitrogen fertilizer costs U.S. farmers approximately $8 billion each year, and excess fertilizer can find its way into rivers and streams, damaging the delicate water systems. Now, a discovery by a team of University of Missouri researchers could be the first step toward helping crops use less nitrogen, benefitting both farmers' bottom lines and the environment. The journal Science published the research this month.

Gary Stacey, an investigator in the MU Bond Life Sciences Center and professor of plant sciences in the College of Agriculture, Food and Natural Resources, found that crops, such as corn, are "confused" when confronted with an invasive, but beneficial, bacteria known as rhizobia bacteria. When the bacteria interact correctly with a crop, the bacteria receive some food from the plant and, simultaneously, produce nitrogen that most plants need. In his study, Stacey found that many other crops recognize the bacteria, but do not attempt to interact closely with them.

"The problem is that corn, tomatoes and other crops have a different response and don't support an intimate interaction with the rhizobia, thus making farmers apply larger amounts of nitrogen than might otherwise be necessary," Stacey said. "Scientists have known about this beneficial relationship since 1888, but it only exists in legume crops, like soybeans and alfalfa. We're working to transfer this trait to other plants like corn, wheat or rice, which we believe is possible since these other plants recognize the bacteria. It's a good first step."

When legumes like soybeans sense a signal from the bacteria, they create nodules where the bacteria gather and produce atmospheric nitrogen that the plants can then use to stimulate their growth. This reaction doesn't happen in other plants.

"There's this back and forth battle between a plant and a pathogen," said Yan Liang, a co-author of the study and post-doctoral fellow at MU. "Rhizobia eventually developed a chemical to inhibit the defense response in legumes and make those plants recognize it as a friend. Meanwhile, corn, tomatoes and other crops are still trying to defend themselves against this bacteria."

In the study, Stacey and Liang treated corn, soybeans, tomatoes and other plants to see how they responded when exposed to the chemical signal from the rhizobia bacteria. They found that the plants did receive the signal and, like legumes, inhibited the normal plant immune system. However, soybeans, corn and these other plants don't complete the extra step of forming nodules to allow the bacteria to thrive.

"The important finding was that these other plants didn't just ignore the rhizobia bacteria," Stacey said. "They recognized it, but just activated a different mechanism. Our next step is to determine how we can make the plants understand that this is a beneficial relationship and get them to activate a different mechanism that will produce the nodules that attract the bacteria instead of trying to fight them."

The study was funded by a grant from the U.S. Department of Energy.??

View the original article here

U.S. approves first artificial pancreas system for diabetics

(Reuters) - The U.S. Food and Drug Administration has approved the first artificial pancreas system for diabetics that reads blood sugar levels and automatically shuts off the flow of insulin.

The device, made by Medtronic Inc, could help the 3 million Americans living with type 1 diabetes better manage their disease, which causes the immune system to destroy cells in the pancreas that make insulin.

Patients suffering from type 1 diabetes, the inherited version of the disease, have to regularly monitor their blood sugar levels and take insulin several times a day.

Too little or too much of insulin can lead to several health problems, ranging from kidney failure and heart disease to brain damage.

The device includes an insulin pump and a glucose sensor that stops insulin delivery when blood glucose reaches a preset level.

The system has been approved for use by diabetics aged 16 years and older. Medtronic said it would conduct a post-approval study that would include children aged 2 years and older.

The Minneapolis, Minnesota-based company said it would begin ramping up production immediately to prepare for a launch in the next few weeks.

The company will also directly follow up with patients and make certain manufacturing changes according to the requirements of the approval and an accompanying warning letter it was issued on September 19.

Medtronic said it has already addressed many of the observations in the warning letter and was committed to resolving the remaining issues as quickly as possible.

(Reporting by Esha Dey and additional reporting by Natalie Grover in Bangalore; Editing by Kirti Pandey)

View the original article here

Chemists slide a splitting catalyst over DNA for first time

Sep. 24, 2013 — Chemists from Nijmegen have developed a catalyst that binds to DNA, slides over it and splits the molecule in particular places. The researchers were able to do this by synthetically modifying a natural catalyst. This finding is a first in the field of chemistry and will help in the selective modification of polymers such as DNA. The results were published online in Nature Chemistry on 22 September.

Roeland Nolte, Emeritus Professor of Organic Chemistry at Radboud University Nijmegen, is the leader of the research project. As he explains, 'Natural enzymes exist that are able to replicate -- that is make a copy of -- DNA. These enzymes consist of a ring to which another enzyme, the replicating catalyst, is clamped. We modified the natural ring and introduced porphyrines, with the result that the system is able to split DNA. We have therefore constructed our own, modifiable, biohybrid catalyst, inspired by nature.'

DNA signposting

The tiny molecular machine is actually not a ring, but a c-shape with a narrow opening. This means that it can easily bind to and slide over DNA. While it is sliding, the machine only splits at a specific sequence: the letters AAA in the DNA -- a repetitive sequence of three adenine molecules. Adenine is one of the four DNA building blocks. 'We can also influence the direction of the catalyst, by sliding it from the left or the right over the DNA', says Nolte. 'We do this by molecularly blocking one side of the DNA so that the catalyst can only move in the other direction.'

Visible splitting positions

The chemists have developed a new technique that shows exactly where the molecular machine has performed the splitting action. The splitting produces a functional group in the DNA that, following treatment with the streptavidin protein, can be visualised using Atomic Force Microscopy (AFM). AFM can be used to investigate the surface of a molecule in detail because the microscope scans the surface using a needle. Using this technique, the researchers were able to detect the splitting locations in the DNA and thereby determine whether or not the machine was indeed moving in the intended direction.

Molecular computer

Molecular machines like this catalyst are very useful in organic chemistry as they make it possible to split DNA in a controlled manner. Nolte explains, 'Our ultimate goal is a fully synthetic catalyst. We would be able to use this in various solvents, whereas the catalyst we currently use only works in a water solution. The synthetic catalyst I have in mind would be a kind of molecular computer that uses the information input to perform precise tasks. We could then use this to modify polymer chains as we please, for example to strengthen them or to store information in them.'

View the original article here

First real-time detector for IV drugs may help eliminate medical errors

Sep. 19, 2013 — Today, computerized smart systems can deliver drugs intravenously in exact volumes to hospital patients. However, these systems cannot recognize which medications are in the tubing nor can they determine the concentration of the drug in the tubing. This lack of precise information can lead to medication errors with serious consequences.

Now, a new optical device developed by a team of electrical and computer engineering students at the University of Illinois at Urbana-Champaign (UIUC) can identify the contents of the fluid in an intravenous (IV) line in real-time, offering a promising way to improve the safety of IV drug delivery. The team, led by Prof. Brian T. Cunningham, interim director of the Micro and Nanotechnology Laboratory at UIUC, will present its work at The Optical Society's (OSA) Annual Meeting, Frontiers in Optics (FiO) 2013, being held Oct. 6-10 in Orlando, Fla.

The vulnerability of IV drug-delivery systems due to human error is a chief concern in hospital safety, Cunningham said. Errors can include incorrect dosage, unintentional substitution of one drug for another, and co-delivery of incompatible drugs.

"Up to 61 percent of all life-threatening errors during hospitalization are associated with IV drug therapy," Cunningham said, citing a recent report. "So for all the really good things hospitals can do, the data shows that mistakes can occasionally happen."

To approach this problem, Cunningham and colleagues turned to the very small -- to structures and processes at the nanoscale (one-billionth of a meter), where novel physical and chemical properties arise. The researchers use a technology called Surface-Enhanced Raman Scattering (SERS), a powerful analytical tool prized for its extreme sensitivity in obtaining molecular signals that can be used to identify chemicals. To determine the identity of a particular IV medication, researchers shine laser light onto a nanostructured gold surface that contains millions of tiny "nano-domes" that are separated from each other by as little as 10 nanometers. The nano-domes are incorporated into the inner surface of IV tubing, where they are exposed to drugs that are dispersed in liquid. They capture the light scattered from drug molecules that are in contact with the nano-domes and use SERS to determine the drug's molecular signature. Finally, they match the signature to known signatures for the drug in order to confirm the presence of a specific medication in the IV line.

While other groups have demonstrated excellent nanostructured surfaces for SERS, those developed by the Cunningham group are unique because they are inexpensively produced on flexible plastic surfaces by a replica molding process with nanometer scale accuracy.

Early data show that the Cunningham group's system can identify medications including morphine, methadone, phenobarbital, the sedative promethazine, and mitoxantrone, which is used to treat multiple sclerosis. The system is extremely sensitive: it can detect drugs in amounts 100 times lower than the clinically delivered drug concentrations commonly used. So far, the researchers have also shown their system can sense a two-drug combination, which has its own unique signature.

The next step is further evaluation for combinations of up to ten drugs being delivered at the same time. Computer algorithms are also being developed to automatically interpret the SERS spectra, and Cunningham's team reports that the system is now being evaluated for possible commercialization.

View the original article here

Weak charge of proton determined for first time

Sep. 17, 2013 — Researchers have made the first experimental determination of the weak charge of the proton in research carried out at the Department of Energy's Thomas Jefferson National Accelerator Facility (Jefferson Lab).

The results, accepted for publication in Physical Review Letters, also include the determinations of the weak charge of the neutron, and of the up quark and down quark. These determinations were made by combining the new data with published data from other experiments. Although these preliminary figures are the most precise determinations to date, they were obtained from an analysis of just 4 percent of the total data taken by the experiment, with the full data analysis expected to take another year to complete.

The weak force is one of the four fundamental forces in our universe, along with gravity, electromagnetism and the strong force. Although the weak force acts only on the sub-atomic level, we can see its effects in our everyday world. The weak force plays a key role in the nuclear reaction processes that take place in stars and is responsible for much of the natural radiation present in our universe.

The Q-weak experiment was designed by an international group of nuclear physicists who came together more than a decade ago to propose a new measurement at Jefferson Lab. They proposed the world's first direct measurement of the proton's weak charge, denoted by the symbol Q^P_W this represents the strength of the weak force's pull on the proton, a measure of how strongly a proton interacts via the weak force. Since the weak charge of the proton is precisely predicted by the Standard Model, which is a well-tested theoretical framework that describes the elementary particles and the details of how they interact, it is an ideal parameter to measure experimentally as a test of the Standard Model.

To perform the experiment, the scientists directed a very intense beam of electrons into a container of liquid hydrogen. The electrons were longitudinally polarized (spinning along or opposite their direction of motion). Electrons that made only glancing collisions with the protons (elastic scattering, where the proton remained intact) emerged at small angles and were deflected by powerful electromagnets onto eight symmetrically placed detectors.

The weak force is far weaker than the electromagnetic force. In classical terms, one might think of this as for every one million electrons that interact with the protons via the electromagnetic force, only one will interact via the weak force. Physicists measured those few weak interactions by exploiting an important difference between the two forces -- the weak force violates a symmetry known as parity, which reverses all spatial directions and turns our right-handed world into a left-handed one. In an opposite-parity world, the electrons spinning with their axes along their direction of motion would interact with protons via the electromagnetic force with the same strength. Where the weak force is concerned, electrons with right-handed spin interact differently than left-handed ones. By keeping all other parameters of the experiment the same, and only reversing the polarization direction of the electron beam, scientists can use the difference or "asymmetry" of the measurements between two polarization directions to isolate the effect of the weak interaction. The goal is to measure this difference, only ~200 parts per billion, as precisely as possible. This precision is equivalent to measuring the thickness of a sheet of paper laid atop the Eiffel Tower.

The initial analysis of the Q-weak experimental data yielded a value for Q^P_W that is in good agreement with the Standard Model prediction. However, the collaboration has 25 times more data than was used in this initial determination. The final result should provide a rigorous experimental test of the Standard Model, providing constraints on new physics at the scale of energies being explored at the Large Hadron Collider at CERN in Europe.

"Readers should view this result primarily as a first determination of the weak charge of the proton. Our final publication will be focused on implications with respect to potential new physics," says Roger Carlini, a Jefferson Lab staff scientist and spokesperson for the Q-weak Collaboration.

The Q-weak experiment was originally approved in January 2002. A nearly year-long installation period for experimental equipment began in 2009, which was followed by a two year period of data collection during 2010-2012.

Numerous technical achievements in the last decade made this experiment possible. These include the high-current, high-polarization, extremely stable electron beam provided by Jefferson Lab's Continuous Electron Beam Accelerator Facility; the world's highest-power cryogenic hydrogen target; extremely radiation-hard Cerenkov detectors; ultra-low noise electronics to read out the signals and precisely measure the beam current; and a system which measures the beam polarization to better than 1 percent using a back-scattered laser. These technical achievements have yielded an astonishingly small total uncertainty of 47 parts per billion for the data published so far.

The Q-weak collaboration consists of 97 researchers from 23 institutions in the U.S., Canada, and Europe. The experiment was funded by the U.S. Department of Energy Office of Science, the U.S. National Science Foundation and the Natural Sciences and Engineering Research Council of Canada. Matching university contributions were also provided by The College of William and Mary, Virginia Tech, George Washington University and Louisiana Tech University. Technical support was provided by TRIUMF, MIT/Bates and Jefferson Lab.

View the original article here

First randomized trial of targeted cancer medicine in all tumor types

Sep. 11, 2013 — A further step along the road to the personalisation of cancer medicine, where treatment is based on the individual molecular characteristics of tumours rather than their primary site, will be presented at the 2013 European Cancer Congress (ECC2013), which starts on Friday 27 September in Amsterdam, The Netherlands.

Dr Christophe Le Tourneau, Head of the Phase I Programme at the Institut Curie, Paris, France, will tell the congress that the SHIVA trial is the first randomised trial to look at patient outcomes after treatments were chosen according to the individual molecular profiles of each person's tumour. It is also the first trial to do this for all tumour types. About 40% of all those taking part in the trial have molecular abnormalities that can be targeted by existing drugs, he will say.

To date, 320 patients from seven comprehensive cancer centres across France have been included in this phase II trial, of whom 60 have been randomised. In the standard arm, the patients received the chemotherapy they would have received if they had not been participating in the trial. All patients had recurrent or metastatic cancer that was unresponsive to standard treatment for their disease.

"Our goal is to have 200 randomised patients," says Dr Le Tourneau. "Although 40% of the 320 patients have a tumour for which targeted drugs are available, some are still on the chemotherapy that was started at the time of the biopsy and therefore we will have to randomise them later. Because we are looking for an effect in different kinds of tumours, we have ruled out the inclusion of any particular type of tumour if this brings the number of randomised patients with this type to over 20% of the total. We have also allowed the inclusion of patients with rare tumours."

Preliminary results of the feasibility study, to be presented at the congress, show that this approach works, the researchers say. The ultimate goal of the phase II trial is to see whether the selection of drugs that target the specific molecular profiles of tumours will improve outcomes for patients.

Once the first 100 patients were included, the researchers looked at the feasibility of a biopsy of a metastasis, since the molecular profile of the primary tumour, if tissue is available, may not be the same as that found in a metastasis. They also investigated the quality of available tumour samples, the proportion of the patients for which the necessary analyses could be undertaken, the proportion for which a molecular abnormality can be identified and for which a targeted therapy exists, and the timeframe needed to establish the tumour profile.

"Recent advances in diagnostics have enabled us to ascertain the molecular profile of tumours in a timeframe which is compatible with good clinical care, but we needed to verify this in our study," says Dr Le Tourneau.

Unlike conventional chemotherapy, molecular targeted agents only work in the presence of their targets. Side-effects are lessened and, in principle, efficacy heightened. One of the problems to date, however, is that such drugs have principally been developed based on the primary location and histology (cellular make-up) of the tumour. This has meant that many potentially promising targeted drugs have failed in early clinical trials simply because they have not induced a response in a sufficient number of patients.

"The history of breast cancer changed beyond recognition with the discovery of the role played by the ErB2/HER2 gene, which is amplified in up to 20% of breast cancers. And we now know that trastuzumab (Herceptin), one of the most widely-used targeted cancer therapies, which targets that gene, is effective in several tumour types and not just in breast when the ERBB2/HER2 gene is amplified or even mutated," says Dr Le Tourneau. "We also know that patient outcomes in the few trials to date where the choice of treatment is based on a molecular abnormality are better than those where the treatment is not matched to the abnormality. What was missing to date is a histology-independent randomised trial comparing molecular targeted treatment with conventional therapy, and this is why I decided to set up the SHIVA trial."

Even today, the researchers say, molecularly targeted therapy for cancer patients is initially prescribed according to the location of the primary tumour. At the end of the trial, analysis of progression-free survival will show whether this practice needs to be changed.

A positive finding would imply the need to make major changes in the way cancer drugs are developed and tested in patients. But this would represent a new and difficult challenge.

"At present we have no data on the efficacy of drugs in patients with the same molecular abnormality but different tumour types, and we also suspect that a treatment effect would not depend on the presence of a single molecular abnormality, but, more likely, on several. However, we believe that it is most likely that, in future, tumour location and histology will no longer be the primary criteria for the prescription of molecularly targeted agents; rather, tumour biology will be the deciding factor," says Dr Le Tourneau. "A positive result from our trial would be an important step forward on the road to personalised medicine."

Professor Cornelis van de Velde, President of ECCO, said: "This ground-breaking randomised trial is very exciting since this is the way to individualise therapy. We have already moved from empirical to stratified treatment, and now we can offer patients personalised treatment based on the understanding of the particular molecular profiles of their tumours in order to select drugs that target a specific profile. The means to determine the individual molecular profiles of tumours will be readily available at low cost in the years to come, and the integration of biopsy-based molecular profiles with individual patient characteristics will enable precision diagnosis to be translated into precision personalised therapies. ECCO will have an important role to play in ensuring the incorporation of molecular biology genetics into clinical multidisciplinary meetings."

View the original article here

Mechanism discovered in first line of immune defense

Sep. 10, 2013 — Scientists from A*STAR's Singapore Immunology Network (SIgN) have discovered a new defense mechanism that the immune system utilises to combat infections. The team's discovery of how a novel protein unexpectedly activates an immune response shows how this mechanism can also be used to get rid of tumour cells. This research was done in collaboration with University Hospital Basel, Switzerland, published in July 2013 in Nature Immunology.

The immune system combats microbes using several strategies, of which early activation of defence is one of the most important. The mechanisms used by the immune system to counterattack microbes often rely on the immediate recognition of microbes, or of cells that have been affected by the infection of microbes.

The team at SIgN led by Prof Gennaro De Libero has identified a novel mechanism of how the immune system readily detects invading microbes and effectively initiates early immune responses, by activating a special class of cells called gamma delta lymphocytes. Gamma delta lymphocytes were discovered more than 30 years ago and had been identified as cells that are capable of early protection as they play a decisive role in the first line of immune defence. However, many studies into discovering the mechanisms of how these cells are activated when microbes attack have been unfruitful.

The team's discovery of a protein called Butyrophilin 3A1 shows how it binds to microbial antigens and hence activates human gamma delta cells. These cells are then able to coordinate an immune response to clear the infection caused by invading microbes.

This protein has also been found to bind antigens that are produced in large amounts in tumour cells, which then activates gamma delta cells against these tumour cells. The discovery of this mechanism thus represents a novel target that will help to eradicate tumours and combat infections.

Prof De Libero said, "The identification of the molecular mechanisms of how human gamma delta cells get activated opens doors to novel opportunities for immunotherapy of infections and tumours."

Prof Philippe Kourilsky, Chairman of SIgN said, "This study is a breakthrough in immunology and also an excellent example of basic science as an important premise to medicine."

Prof Laurent Renia, Acting Executive Director of SIgN said, "We are delighted that this excellent science has paved the way for many others in immunology and other fields. I believe that these findings present great promise in developing new treatments for cancer therapy and infectious diseases."

View the original article here