Tuesday, January 21, 2020

Remarkable New T-Cell Discovery Can Kill Several Cancer Types in The Lab

The discovery of a new kind of immune cell receptor could pave the way for a new type of T-cell cancer therapy that can attack a diverse range of cancers in human patients without requiring tailored treatment.

The researchers behind the discovery emphasise that testing is still at an early stage, having been conducted only in mice and in human cells in the lab, not yet in living patients. But the preliminary results are promising, and suggest we could be on the verge of a significant advancement in T-cell therapies.

To understand why, let's backtrack a little on what T-cells are, and what T-cell therapies do, because they're still very much an emerging field of treatment in oncology.

T-cells are a type of white blood cell involved in the function of our immune system. When T-cells are activated by coming into contact with defective or foreign cells in the body, they attack them, helping us fight off infection and disease.

In T-cell therapy – the most common form of which is called CAR-T (for Chimeric Antigen Receptor T-cells), scientists hijack and augment this natural function of T-cells to steer them towards tumour cells in particular.

In CAR-T treatments, doctors extract T-cells from patients' blood, genetically engineering them in the lab to make them specifically identify and target cancer cells. The edited T-cells are then multiplied in the lab before being administered to patients.


Some of the limitations of the CAR-T technique are that the edited T-cells are only able to recognise a few kinds of cancer, and the entire therapy needs to be personalised for different people because of a T-cell receptor (TCR) called human leukocyte antigen (HLA).

HLA is what enables T-cells to detect cancer cells, but it varies between individuals. And that's where this new discovery comes in.

In the new study, led by scientists at Cardiff University in the UK, researchers used CRISPR–Cas9 screening to discover a new kind of TCR in T-cells: a receptor molecule called MR1.

MR1 functions similarly to HLA in terms of scanning and recognising cancer cells, but one big difference is that, unlike HLA, it doesn't vary in the human population – which means it could potentially form the basis of a T-cell therapy that works for a much broader range of people (in theory, at least).

We're not there yet; but preliminary experiments in the lab involving MR1 are indeed promising, although we need to be aware that the results need to be replicated safely in clinical trials before we can confirm this is a treatment suitable for humans.


In lab tests using human cells, the MR1-equipped T-cells "killed the multiple cancer cell lines tested (lung, melanoma, leukaemia, colon, breast, prostate, bone and ovarian) that did not share a common HLA," the authors write in their paper.

Tests upon mice with leukaemia – in which the animals were injected with the MR1 cells – revealed evidence of cancer regression, and led to the mice living longer than controls.

Right now, we don't yet know how many types of cancers a technique based on this receptor might treat. That said, the early results certainly suggest a diverse range could be susceptible, according to the study.

If these sorts of effects can be replicated in humans – something the scientists hope to begin testing as early as this year – we could be looking at a bright new future for T-cell treatments, experts say.

"This research represents a new way of targeting cancer cells that is really quite exciting, although much more research is needed to understand precisely how it works," says research and policy director Alasdair Rankin from blood cancer charity Bloodwise, who was not involved in the research.

To that end, the next step for the team – in addition to organising future clinical trials – will be learning more about the mechanisms that enable MR1 to identify cancer cells at a molecular level.

There's a lot more to learn here before we can truly proclaim this is some kind of universal cancer treatment, but there certainly look to be some exciting discoveries on the horizon.

"Cancer-targeting via MR1-restricted T-cells is an exciting new frontier," says senior researcher and cancer immunotherapy specialist Andrew Sewell.

"It raises the prospect of .. a single type of T-cell that could be capable of destroying many different types of cancers across the population. Previously nobody believed this could be possible."

The findings are reported in Nature Immunology.


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Monday, July 24, 2017

A Vaccine For Type 1 Diabetes Begins Human Trials in 2018

A prototype vaccine, decades in the making, that could prevent type 1 diabetes in children is ready to start clinical trials in 2018.

It's not a cure, and it won't eliminate the disease altogether, but the vaccine is expected to provide immunity against a virus that has been found to trigger the body's defences into attacking itself, potentially reducing the number of new diabetes cases each year.

Over two decades of research has already provided solid evidence linking a type of virus called coxsackievirus B1 with an autoimmune reaction that causes the body to destroy cells in its own pancreas.

The type 1 form of diabetes – not to be confused with the more prevalent type 2 variety that tends to affect individuals later in life – is a decreased ability to produce the insulin used by the body's cells to absorb glucose out of the blood.

This loss of insulin is the result of pancreatic tissue called beta cells being destroyed by the body's own immune system, often within the first few years of life.

It's something of a mystery as to why the body identifies beta cells as foreign, though there could be a genetic link producing variations of human leukocyte markers, which act as the cell's 'ID tags'.

No doubt it's complex, and there are numerous ways this process can be triggered. One example established by virologist is an infection by a type of enterovirus.

Enteroviruses are nasty pieces of work; you might be most familiar with polio, but they can also cause hand, foot and mouth disease, meningitis and myocarditis. There has been suspicion of a link between this group of pathogens and diabetes for a number of years, but it took time to nail down the prime suspects.

In 2014, the team used a pair of studies on children with type 1 diabetes to show that at least one of the six viruses in the B group of coxsackieviruses was associated with the condition.

Enteroviruses are surprisingly common in newborns, with the study finding that around a quarter of the 444 known enterovirus infections in
2007 were caused by coxsackievirus B1 (CVB1).

And for some of those children, it could have been the start of a life-long, incurable condition.

"One can estimate from the generated data that less than 5 percent of CVB1-infected children go on to develop type 1 diabetes," the researchers wrote in their 2014 study.

That might not seem like a lot, but it does suggest each year hundreds of infants around the globe develop type 1 diabetes. If the other members of the CVB group also contribute to beta cell autoimmunity – which they might – the numbers could be higher.

If all goes well, this newly developed vaccine could put a stop to that.

"Already now it is known that the vaccine is effective and safe on mice," says the author.

"The developing process has now taken a significant leap forward as the next phase is to study the vaccine in humans."

Pre-clinical trials are of course just the first step. The next phase will involve testing on healthy adult humans, just to map out any complications.

As a bonus, the vaccine could help reduce other enterovirus infections.

"Additionally, the vaccine would protect from infections caused by enteroviruses such as the common cold, myocarditis, meningitis and ear infections," says the author.

It could be another eight years before we see whether the vaccine does what it's supposed to do, so we shouldn't be expecting anything revolutionary too soon.

Earlier this year, researchers identified an immature cell in the pancreas which can potentially be encouraged to take up the job of lost mature beta cells.

There will be no single cure, treatment, or prevention which will gives us a diabetes-free world.

Between 20 and 40 million people worldwide live with type 1 diabetes. A vaccine like this might not end the disease, but if it works it's certainly going to be a big step forward.
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Saturday, May 06, 2017

Finally Uncovered a Key Mechanism Behind Devastating Autoimmune Diseases

Researchers have discovered how certain molecules in the body can cause autoimmune diseases, showing the first mechanistic evidence for why they actually occur.

Autoimmune diseases are a problem for over 50 million Americans, and although we are starting to understand more about how to ease symptoms, we still don't fully understand the basics.

"We have known that in autoimmune diseases there are T-cells that make us susceptible to disease and T cells that protect us from disease," says one of the researchers,Richard Kitching, from Monash University in Australia.


"Now we know how this happens; it opens the field for new and more targeted treatments to specific diseases."

The new research has found an important interaction between two genes, which helps T cells communicate the correct defensive signals to prevent them attacking the body.

But let's back up a bit, because exactly is an autoimmune disorder?

Usually, our immune system is very adept at attacking 'foreign' invaders such as viruses, bacteria, or other micro-organisms that shouldn't be there. But in autoimmune disorders, the immune system begins treating a part of your body as 'foreign' too.   

In type 1 diabetes it's destroying the cells that produce insulin, and in rheumatoid arthritis the immune cells attack joints.

Researchers investigated Goodpasture syndrome in mice models, a rare condition caused by the immune system attacking the basement membrane in lungs and kidneys.

Past studies have shown that there are particular proteins, or molecules, in the body that makes you more or less likely, depending on the molecule, to get autoimmune diseases.

The Human Leukocyte Antigen (HLA) system is a series of genes that code for the proteins that help the immune system. Some HLA molecules are on the surface of T cells, and will show off tiny bits of invaders to other immune cells to help them destroy it.

"Certain immune molecules, called HLA molecules, are associated with an increased genetic risk to cause autoimmunity, whereas other HLA molecules can protect from disease," says senior researcher, Jamie Rossjohn from Monash University.

For example, some versions (or allelles) of a HLA molecule called DR15 have been shown to increase disease risk of Goodpasture syndrome, multiple sclerosis, and other autoimmune conditions.

Another molecule, called HLA-DR1, has also been linked to a number of autoimmune conditions.

What the researchers didn't know until now is what the mechanism of these molecules actually was, and why it was causing an increase in autoimmune diseases.

The researchers took mice that had been bred to express the human DR15 gene, or the human DR1 gene, and discovered that the DR15 mice began to develop Goodpasture syndrome, but those with just DR1 or both molecules didn't.

"In Goodpasture's disease, when the molecule DR15 is present, it can select and instruct T cells to attack the body. If alone in our body these damaging cells can attack the body's tissues, resulting in very ill patients," says Kitching.

"But when people also have the protective DR1 molecule present these T cells are held at bay and can be overturned."

To be clear, this research has only been done in mice models, but it's an important step forward in understanding how and why our immune system starts seeing the body as a threat, and the researchers are hopeful that the results will lead to tangible outcomes for patients.

"These particular protective immune cells are specific and are extremely powerful,"Kitching says.

"So, if we can encourage them to develop in the body, or expand people's cells outside the body and inject them back into those with disease, this could result in better and more targeted treatments for autoimmune diseases."

The research has been published in Nature. 

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Wednesday, August 21, 2013

Cardiac Sarcoidosis:Causes, Types, Diagnosis, Treatment

Cardiac Sarcoidosis: Causes
The exact cause of sarcoidosis is unknown. Granulomas appear to be the result of an immune system response to an unidentified trigger. Infections agents as well as environmental exposures are thought to be possible precipitants for this immune response; however, no clear triggers or causes have been identified. Genetic mutations in white blood cell proteins (called human leukocyte antigens, or HLA) as well as chemicals that control inflammation (called cytokines) have also been linked to sarcoidosis.

Cardiac Sarcoidosis: Types
Cardiac sarcoidosis (CS) can take many forms, some benign and others serious.

Heart Rhythm Disorders: Interference of electrical movement through the heart is the one of the  complications of CS and can include complete heart block which can be life threatening. Alternatively, fast heart rhythms such as atrial flutter, atrial fibrillation, supraventricular tachycardia, and ventricular tachycardia can be present. Ventricular tachycardia occurs in almost 25 percent of CS patients and is of particular concern since it can lead to sudden cardiac death. These possible complications may occur suddenly without warning.
Heart Failure: Heart failure is another common complication of CS. Sarcoidosis can cause the heart muscle to weaken and/or stiffen, leading to fluid retention in the lungs, abdomen, and lower extremities. In extreme cases, an aneurysm can form due to weakening of the heart wall. Granulomas can also infiltrate the heart valves, causing leaky valves also resulting in heart failure.
Coronary Disease: Although rare, CS can cause inflammatory disorder of the heart arteries called vasculitis. In severe forms, vasculitis can lead to coronary artery blockages, chest pain and, ultimately, heart attacks.
Pericardial Disease: Inflammation of the sack around the heart, called pericarditis, is another rare but important form of CS.

Diagnosing cardiac sarcoidosis (CS) can be very challenging. There are no widely accepted guidelines for either screening or diagnosing CS. Moreover, the current available diagnostic tests are variable in their ability to detect CS. Because of its devastating nature, most patients with other forms sarcoidosis are screened for CS.

Initial cardiac evaluation may include an EKG, a signal averaged EKG, an echocardiogram and a Holter monitor (extended EKG). Additional imaging tests may include single positron emission computed tomography (SPECT), positron emission tomography (PET) and cardiac MRI. A positive heart biopsy confirms CS, but a heart biopsy may more often be negative or normal even when there is sarcoid in the heart, especially if heart function is normal.

Cardiac Sarcoidosis: Treatment
Controversy exists as to the best treatment for cardiac sarcoidosis (CS). However, treatment is generally directed at minimizing the inflammation associated with CS and protecting against the life-threatening complications.

Because of their anti-inflammatory properties, corticosteroids (cortisone, prednisone and methylprednisolone) are the first-line therapy. When patients cannot take steroids, or when combination therapy is necessary, medications such as methotrexate, azathioprine, mycophenolate and antimalarials are used.

Additional therapies for specific CS-related heart disorders may be necessary. For example, heart rhythm disorders such as complete heart block typically require placement of a permanent pacemaker, whereas ventricular tachycardia generally requires internal cardiac defibrillator (ICD) placement.


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