How infection site affects the immune system

A new study by scientists at the Gladstone Institutes shows that infection sites could affect the immune system's response to a virus and the way the virus spreads through the body. The researchers focused on common routes of sexual transmission of viruses, such as the lower female reproductive tract and the lower gastrointestinal tract that includes the large intestine and the anus.

These mucosal barriers-the body's openings lined with a membrane called mucosa are responsible for distinguishing between harmless bacteria that normally reside in human and potentially dangerous pathogens, as well as other substances, such as food or sperm. Human body is constantly trying to balance between tolerating harmless elements and defending against the threats.

Reseachers discovered that the body's reaction is different based on the infection site. They showed that the vaginal and rectal cavities activate a distinct immune response to the same pathogen. To conduct the study, research team created a new model of viral infection through the rectum that uses lymphocytic choriomeningitis virus (LCMV), a rodent virus often used in research to model other pathogens. They then compared their findings to their previous work on vaginal infection by LCMV.

In 2016, they showed that vaginal infection causes a delayed response by protective cells. As a result, the immune system takes longer to clear the virus from the female reproductive tract. They also noticed that the virus stayed in the vagina and didn't spread to other parts of the body. In contrast, the new study indicates that, after infection through the rectum, the virus rapidly spreads throughout the body. The scientists also found that the virus wasn't being carried through the blood. Instead, LCMV infects the body's own immune cells, which in turn spread the virus systemically. Interestingly, this is the same dissemination process used by the HIV virus.

The initial immune response elicited depends on the route of infection, and can actually dictate the dissemination of the virus. The researchers revealed that mucosal barriers have different tolerance mechanisms that affect the immune system's response to invading pathogens. Once a virus breaches one of the barriers, early events in the body's response to that virus can play a key role in determining the outcome of an infection.
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Bacteria prevent transmission of Zika and Dengue viruses

Scientists at the University of Glasgow's MRC Centre for Virus Research opens in new window (CVR) have found a bacterial strain which blocks dengue and Zika virus transmission from mosquitoes. In a new study, published in PLOS Pathogens opens in new window, the scientists show that a novel strain of the inherited bacteria, called Wolbachia, strongly blocks transmission of dengue and Zika virus in infected mosquitoes. This finding could offer a potential alternative to strains already being tested as virus control tools.

The scientists have already carried out the research in the mosquito species Aedes aegypti, notorious for spreading several dangerous human viruses, including dengue, Zika and chikungunya. Previous research in the scientific community has shown that transmission of these viruses among mosquitoes is stalled if the flies are deliberately infected with one strain of Wolbachia bacteria. With this knowledge, several countries are testing whether infecting local mosquito populations with Wolbachia could lead to lower rates of viral disease in humans.

The MRC scientists in Glasgow found that a novel strain-called 'wAu' – is more effective for virus transmission blocking than the strains currently being used. The effect is emphasised in hot, tropical climates where there is a high prevalence of these diseases. The Wolbachia transmission blocking strategy shows great promise for the control of mosquito-borne viruses, and is now starting to be deployed on a large scale in a number of tropical countries.

The results with the wAu strain showed by far the effective transmission blocking for all the viruses we tested, and it provides an exciting new option to explore for disease control programmes. Several Wolbachia strains have already been tested in the field, but there is evidence to suggest that some strains may not block transmission very effectively or may not be inherited efficiently at high ambient temperatures. In the new study, the research team performed laboratory experiments to test the potential promise of alternative Wolbachia strains.

The researchers introduced four Wolbachia strains into Aedes aegypti mosquitoes, which do not naturally carry these anthropod-infecting bacteria. Two of the strains, wMel and wAlbB had already been evaluated in prior studies, and the scientists wanted to compare their effects with those of two novel strains, wAu and wAlbA.

The analysis revealed particularly promising results for strain wAu. After feeding on blood infected with dengue or Zika virus, mosquitoes infected with wAu had lower levels of viral RNA in their body tissue than did mosquitoes infected with the other strains. wAu also showed very high rates of inheritance, including under high-temperature conditions. The aim is to reduce and block the transmission of pathogens by releasing specific insect disease vectors.
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Onions could fight antibiotics resistance

A type of onion could fight against antibiotic resistance in cases of tuberculosis TB, a UCL and Birkbeck-led study suggests. Researchers believe the antibacterial properties extracted from the Persian shallot could increase the effects of existing antibiotic treatment.

The study was led by Dr. Sanjib Bhakta of Birkbeck, University of London and UCL's Professor Simon Gibbons, who worked with a team of scientists from Birkbeck, UCL, the University of Greenwich, the University of East London and Royal Free Hospital. When a patient has a bacterial infection, they may be prescribed an antibiotic. In the case of TB, they will likely be prescribed a cocktail of four antibiotics including Isoniazid and Rifampicin – but increasingly, the pathogens in bacterial infections are developing resistance to antibiotic drugs.

This means the drug loses its ability to effectively control or kill harmful bacteria, and is free to grow and cause further damage to the patient which, can be passed along to the population at large. Therefore, there is a pressing need to develop new classes of antibacterials to combat antibiotic resistance, which this research may help progress. The team investigated extracts of bulbs from Allium Stipitatum – also known as the Persian shallot and used as a staple part of Iranian cooking- and its antibacterial effects.

They synthesised the chemical compounds present in these plants in order to better understand and optimise their antibacterial potential. They tested four different synthesised compounds, all of which showed a significant reduction in the presence of the bacteria in the multidrug-resistant tuberculosis-the most promising candidate of which, with highest therapeutic index, inhibited growth of the isolated TB cells by more than 99.9%.

The team concluded that the chemical compounds may work as templates for the discovery of new drug treatment to combat strains of tuberculosis, which have previously developed resistance to anti-bacterial drugs.Natural products from plants and microbes have enormous potential as a source of new antibiotics. Nature is an amazingly creative chemist and it is likely that plants such as the Persian shallot produce these chemicals as a defence against microbes in their environment.
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HIV-1 genetic diversity is higher in vaginal tract than in blood

The genetic diversity of human immunodeficiency virus type 1 (HIV-1) is higher in the vaginal tract than in the blood stream during early infection. When HIV-1 is transmitted from a man to a woman via intercourse, it must penetrate and infect various vaginal layers before reaching the blood.

Previous research has shown that, within a patient, systemic infection is usually established by a single genetic variant of HIV-1 in the blood. However, scientists hypothesize, the vaginal tract may initially harbor a genetically diverse HIV-1 population that is then filtered down to a single variant along the path to the blood stream.

Katja Klein of the University of Western Ontario, Canada, and colleagues conducted the first study to compare HIV-1 genetic diversity between the vaginal tract and the blood in newly infected people. They collected and applied next-generation deep sequencing to HIV-1 viruses isolated from the vaginal tract and blood plasma of women within seven months of infection.

This analysis revealed that each patient's vaginal tract generally harbored a diverse range of HIV-1 genetic variants (a mean of 5.7), while the blood had much lower genetic diversity (a mean of 1.7 variants). These results held true regardless of a patient's HIV-1 subtype, use of hormonal contraceptives, or number of sex acts or partners.

All samples in the study were collected at least one month after initial infection, and the researchers acknowledge the possibility that genetic diversity in the vaginal tract may have arisen post-infection. However, they point out that this is unlikely, given that similar diversification was not seen in the blood stream.

These findings present new evidence in support of the idea that a genetic bottleneck winnows out many genetic variants of HIV-1 between the vaginal tract and the blood during early infection. This could improve understanding of the transmission process, thereby informing efforts to develop vaccines and other therapies to prevent against HIV-1 infection.

Like many infectious pathogens and diseases, human mucosal layers have evolved to produce protective molecules, accommodate good microbes and keep the bad ones out of the blood stream
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Bacteria obtain resistance from competitor

Bacteria not only develop resistance to antibiotics, they also can pick it up from their rivals. In a recent publication in Cell Reports, Researchers from the Biozentrum of the University of Basel have demonstrated that some bacteria inject a toxic cocktail into their competitors causing cell lysis and death. Then, by integrating the released genetic material, which may also carry drug resistance genes, the predator cell can acquire antibiotic resistance.

The frequent and sometimes careless use of antibiotics leads to an increasingly rapid spread of resistance. Hospitals are a particular hot spot for this. Patients not only introduce a wide variety of pathogens, which may already be resistant but also, due to the use of antibiotics to combat infections, hospitals may be a place where anti-microbial resistance can develop and be transferred from pathogen to pathogen. One of these typical hospital germs is the bacterium Acinetobacter baumannii. It is also known as the "Iraq bug" because multidrug-resistant bacteria of this species caused severe wound infections in American soldiers during the Iraq war.

The emergence and spread of multidrug resistance could be attributed, among other things, to the special skills of certain bacteria: Firstly, they combat their competitors by injecting them with a cocktail of toxic proteins, so-called effectors, using the type VI secretion system (T6SS), a poison syringe. They are able to uptake and reuse the released genetic material. In the model organism Acinetobacter baylyi, a close relative of the Iraq bug, Prof. Marek Basler's team at the Biozentrum of the University of Basel, has now identified five differently acting effectors. Some of these toxic proteins kill the bacterial competition very effectively, but do not destroy the cells.

The predator bacteria take up the released DNA fragments. If these fragments carry certain drug resistance genes, the specific resistance can be conferred upon the new owner. As a result, the antibiotic is no longer effective and the bacterium can reproduce largely undisturbed. Pathogens with such abilities are a major problem in hospitals, as through contact with other resistant bacteria they may accumulate resistance to many antibiotics -- the bacteria become multidrug-resistant. In the worst case, antibiotic treatments are no longer effective, thus nosocomial infections with multidrug-resistant pathogens become a deadly threat to patients.

The T6SS, as well as a set of different effectors, can also be found in other pathogens such as those which cause pneumonia or cholera. Interestingly, not all effectors are sufficient to kill the target cell, as many bacteria have developed or acquired antitoxins -- so-called immunity proteins. Antibiotics and anti-microbial resistance have existed for a long time. They developed through the coexistence of microorganisms and enabled bacteria to defend themselves against enemies or to eliminate competitors. This is one of the ways in which bacteria can conquer and colonize new environmental niches. With the use of antibiotics in medicine, however, the natural ability to develop resistance has become a problem. This faces researchers with the challenge of continually developing new antibiotics and slowing down the spread of drug resistance.
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Blood clotting disorder causes miscarriages

Women with the rare autoimmune disorder Antiphospholipid syndrome APS are prone to successive pregnancy losses. APS causes abnormal blood clots in the arteries or veins along with the risks that go with clotting, including stroke and Deep Vein Thrombosis. For pregnant women the effects of the disorder can be devastating, causing about half of them to be at risk of sequential miscarriages, spontaneous abortions or premature births.

Researchers have identified a protein that may protect against APS miscarriages. The researchers used purpose-bred mice injected with the antibodies that cause the condition to test the effects of the proteins CD39 and CD73, which work together to produce a molecule known as adenosine.

Adenosine has anti-inflammatory, anti-oxidant and anti-clotting properties. APS occurs when there is an increased level of circulating antibodies-the proteins designed to attack invading pathogens in the system but which, in the case of autoimmune diseases such as APS, attack the body's own cells. It was known that these antibodies were linked to clotting but not all patients with them go on to have APS.

The rates of miscarriages were compared in mice that lacked CD39 and CD73, in normal mice, and in mice with large amounts of the two proteins in their blood. The study found, as hypothesised, that mice that lacked CD39 and CD73 both had increased rates of miscarriages. Those with no CD39 lost 20% of fetuses. That is a six-fold increase compared with normal mice which lost 3.67% of fetuses. The mice with no CD73 had a three-fold increase. Mice with large amounts of CD39 had reduced miscarriage rates compared to those without it.
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The secrets of Ebola

In a comprehensive and complex molecular study of blood samples from Ebola patients in Sierra Leone. Conducting a sweeping analysis of everything from enzymes to lipids to immune-system-associated molecules, the teamfound 11 biomarkers that distinguish fatal infections from nonfatal ones and two that, when screened for early symptom onset, accurately predict which patients are likely to die.

Health workers collected blood samples from patients after they were diagnosed with Ebola and at multiple points thereafter.They obtained 29 blood samples from 11 patients who ultimately survived and nine blood samples from nine patients who died from the virus. For comparison, the research team also obtained blood samples from 10 healthy volunteers with no exposure to Ebola virus.
"Our team studied thousands of molecular clues in each of these samples, sifting through extensive data on the activity of genes, proteins and other molecules to identify those of most interest.

The team found that survivors had higher levels of some immune-related molecules, and lower levels of others compared to those who died. Plasma cytokines, which are involved in immunity and stress response, were higher in the blood of people who perished. Fatal cases had unique metabolic responses compared to survivors, higher levels of virus, changes to plasma lipids involved in
processes like blood coagulation, and more pronounced activation of some types of immune cells.

Pancreatic enzymes also leaked into the blood of patients who died, suggesting that damage from these enzymes contributes to the tissue damage characteristic of fatal Ebola virus disease. The study showed that levels of two biomarkers, known as L-threonine (an amino acid) and vitamin D binding protein, may accurately predict which patients live and which die. Both were present at lower levels at the time of admission in the patients who ultimately perished.

When Ebola virus leads to death, experts believe it is because of overwhelming viral replication. Symptoms of infection include severe hemorrhaging, vomiting and diarrhea, fever and more. In the current Ebola study, the team found that many of the molecular signals present in the
blood of sick, infected patients overlap with sepsis, a condition in which the body in response to infection by bacteria or other pathogens mounts a damaging inflammatory reaction.
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New mechanism for battling influenza

A human protein called TRIM25, which was recently discovered to play an important role in the human immune response to flu infection; and a protein called NS1 present in all strains of the influenza.

TRIM25 acts earlier than previously believed, latching on to a critical and unique flu virus structure like a molecular clamp to keep the virus from replicating as soon as TRIM25 detects this unique structure. NS1 produced by the flu virus can block this function of TRIM25, enabling flu to circumvent the immune response and cause infection.

TRIM25 fought off flu by switching on interferon response- a complex signaling pathway that strengthens cells through the body to fight off pathogens. But not all strains of influenza block this interferon signaling pathway. TRIM25 is also a restriction factor - a special protein present in the fastest-acting arm of the immune system, before spreading infection. Restriction factors lie in wait to detect a virus in the cells.

Flu uses its NS1 protein to evade TRIM25's early flu-fighting response, the researchers infected transgenic cell lines loaded with nonhuman primate versions of TRIM25 with the human influenza virus. They discovered that the cells fought off the virus far better than human versions of the TRIM25 protein.

TRIM25 has the capacity to crush influenza, the researchers combined purified TRIM25 with purified viral ribonucleoproteins (vRNPs)- eight-piece protein chains that house the influenza genome and used state-of-the-art electron microscopy to take pictures of what happened.

They found that TRIM25 appears to swiftly recognize the unique structure of vRNPs and clamps down on them to keep them from replicating inside the cell. Other experiments confirmed that the NS1 protein in flu virus inhibits this function. They also found that TRIM25 is also present in the cell nucleus, which is the same cellular location where flu replication occurs.
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Links between microbiomes and autoimmune disorders

Bacteria in human body have all kinds of positive effects on our health, the bacteria in the gut have many beneficial functions. They help in digestion, prevent infection by pathogens and strengthen immune system to fight diseases.

A new function of a protein in the gut microbiome reveals potential impacts for those who suffer from inflammatory bowel disease IBD. A protein expressed by gut bacteria called Bacteroides works to prevent IBD by rapidly recruiting white blood cells to kill a cell of the immune system that is responsible for orchestrating IBD.

However, there is a flipside to the protein's call for help. In some people, the white blood cells overreact to the presence of the IBD bacteria. This is what causes problems like IBD, it's not the bacteria itself, but the immune system's severe reaction triggered by the protein.

These same overstimulated white blood cells are also the cells that cause other autoimmune disorders like diabetes, this discovery demonstrates the effect the gut microbiome has on the immune system and unearths a novel mechanism through which changes in the gut microbiome can increase the risk of autoimmune disorders.
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Links between gut bacteria and autism

According to the latest research, gut bacteria could cause spectrum disorder. Pathogens in the stomach alter the brain's development and may increase risk of suffering from the spectrum disorder.

Links between the brain, gut and stress hormone cortisol can influence how messages are passed in the body, which may cause autistic symptoms.

Changes in neurometabolites in childhood can have dangerous effects on brain development. Collection of bacteria, fungi, and viruses living in humans gut may be responsible for the disorder.

Autism may be corrected by changing of diet, taking probiotics and adopting a gluten-free lifestyle which may improve social behaviour and ability to express emotions in autistic people.

Leaky gut releases toxins and even undigested food enter the bloodstream and travel to the brain, which may cause autism symptoms. Probiotics can change this by enhancing the gut's lining.
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DNA sensor and cancer immunotherapy

Tumors stressed by cancer immunotherapy release their mitochondrial DNA into the closer immune cells, causing a host alert system. The chemical alert through the molecule cGAS is an important immune-system sensor for DNA that is in the interior of cells, the cytosol, where DNA should not exist. 

 cGAS connected the innate immune system, which senses initial threats; and the adaptive immune system, which amplifies the anti-tumor response after getting the alert from the innate immune system. The adaptive system battles recurring threats from pathogens. Checkpoints are molecular barriers that cancer cells produce to make themselves undetectable to the immune system. The plan of immunotherapy is to make the cancers detectable.

Current immune checkpoint blockade therapy has been life-extending for many people. The drug targets CD47, a cell surface protein highly expressed in some tumor cells. CD47 signal to block immune cells from killing the cancer cells. cGAS as an innate immune sensor of DNA led to speculation that inhibition of cytosolic DNA sensing could represent a strategy tumor cells used to evade the immune system.

CD47 is found in every cell of the body, and it has long been known that many kinds of cancer cells produce higher amounts of CD47 than healthy cells. CD47 signal helps cancer cells evade detection from the immune system's killer T-cells.

The higher the levels of CD47 found in tumors, the poorer the prognosis for many cancers. Using mouse cells,
the researchers discovered that when cancer cells are stressed by an experimental anti-CD47 immunotherapy, it leaks DNA into nearby dendritic cells, which present antigens to killer T-cells and are considered a bridge between the innate and adaptive immune systems.

 The DNA sensor cGAS sounds the alarm inside those dendritic cells, setting off a signaling cascade that alerts the
immune system and unleashes the cancer-killing T-cells. cGAS is essential for cancer immunotherapy by immune checkpoint blockade. Activating DNA comes from the mitochondria of the cancer cells. Tumor-originated mtDNA was recognized by the DNA sensor cGAS in dendritic cells during anti-CD47 treatment.

 cGAS-STING-IRF3 signaling pathway plays a critical role to drive robust innate and adaptive immune response upon anti-CD47 therapy. Understanding this mechanism of anti-CD47 therapy may make it possible to design new combination strategies to improve current immune checkpoint blockade therapies by modulating the innate sensing of mtDNA.
       

Targeted cell metabolism can improve immune system

Immune system can become so over-activated when fighting infections that the resulting inflammatory response can lead to death. Excessive response by the immune system can be modulated by targeted manipulation of the sugar metabolism to produce an immune response that eliminates the pathogens without causing any harmful to the immune system.

Using 2-Deoxy-D-glucose 2-DG during the infection make this possible, adding 2-DG, that prevents glycolysis, causes increased production of interleukin-12 IL-12, a pro-inflammatory cytokine, while suppressing the production of interleukin-10, an anti-inflammatory cytokine.

IL-12 triggers a specific T-cell immune response, which is part of the cellular immune response, to specifically boost the defence mechanisms that serve to eliminate intracellular pathogens like listeria. Addition of 2-DG changes the nature of the immune response and the intensity of the inflammatory process, inflammation is controlled so that the immune system is able to manage the situation without allowing the infection to leads to a deadly outcome.

This prevents excessive inflammatory responses, following addition of of 2-DG, only p40 is upregulated, while no p35 is produced. This modified cytokine profile, there is also a simultaneous increase in IL-23 expression which could subsequently bring about modified recruitment of immune cells and hence have a decisive influence on the intensity of the immune response.

The metabolic increased production of activating mediators with simultaneous inhibition of immunosuppressive mediators. Manipulation of the sugar metabolism and associated modulation of the immune system could open up new options for treating specific infectious and autoimmune diseases
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How immune cells kill bacteria

In order to kill a pathogen invading the human body, T cells bind to it through T cell receptors TCR. This binding initiates the formation of a microcluster that includes hundreds of TCR molecules.
These microclusters are very important to initiate and sustain the immune signal.

TCR function by forming a complex (TCR/CD3) with CD3,CD45, on the other hand, is not part of the complex, but it regulates the formation of the clusters.
Single molecule imaging was used to trace the movement of CD3 and CD45 around the microclusters. The researchers discovered that the dynamics of the two molecules depended on their location relative to the microclusters and could be used to determine their interactions with the microclusters.

 The kinetics showed CD3 and CD45 could take either a fast or slow mobility state. Inside the microcluster, the slow mobility state was dominant, reflecting stronger interactions between the two molecules and the microcluster. Outside and at the boundary, however, the fast mobility state was dominant. Yet a small fraction of molecules behaved according to the slow mobility state, suggesting that TCR nanoclusters exist at the outside or boundary of the microcluster.

 The dynamics and kinetics at the single molecule level is very important for defining the molecular mechanisms of biological functions. Along with the new development of biopharmaceuticals related to immune control, elucidation of the mechanism of T cell activation is becoming more important in clinical application.
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Testicular macrophages guard fertility

At birth, human immune system differentiate between native cells pathogenic cells. But in males, sperm develop at puberty, the sperm may be recognized as foreign cells by some elements of the immune system.

Testicular macrophages are immune cells that rush to the defense of sperm. By releasing specific molecules, these guardians of fertility prevent other immune system agents from getting to the testes.

Macrophages migrate to sites of infection and phagocytose pathogens. They also modulate immune system activity to ensure proper organ function and regeneration.

They may arise from embryonic progenitors or bone marrow cells in adults. The testis is divided into two compartments; one of testicular macrophage is in the interstitial spaces, where testosterone-producing Leydig cells are located.

These interstitial macrophages are of embryonic origin: they are present at birth. The other is peritubular - it is located on the surface of the seminiferous tubules that house sperm cell precursors.

Each macrophage population has distinctive cellular markers. The researchers used a new cell tracing method to follow the movement of peritubular macrophages from the bone marrow to the testes in mice.

They discovered that these macrophages only appear two weeks after the birth of mice, the same duration in human. Once they have been established in the testes, macrophages remain there for the rest of their lives.
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How to rearrange immune system cells

Immune system imbalanced due to overly-active cells or cells that suppress its function can cause different diseases. Manipulating the function of  T cells, could restore the immune system's balance and create new treatments for any diseases.

Pro-inflammatory cells that boost the immune system can be rearrange into anti-inflammatory cells that suppress disease. Effector T cells activate the immune system to defend human body against different pathogens while regulatory T cells control the immune system and prevent it from attacking healthy parts of its cells.

This rearrangement can be used in the treatment of autoimmune diseases and immuno-oncology therapies. The use of molecule drug that can rearrange effector T cells into regulatory T cells is very important for strengthening  immune systems. This metabolic mechanism changes one cell type into another.

In autoimmune disease, effector T cells are activated and cause damage to the body. Changing these cells into regulatory T cells could reduce the hyperactivity and return balance to the immune system. This rearrangement could improve therapies using stem cells, promotes immune tolerance and prevents the body from rejecting newly-transplanted cells.

Some cancers control regulatory T cells to suppress the immune system and allowing tumors to grow without detection. This process can activate the immune system, recognize cancer cells and attack them.
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New way of generating human antibody

Antibodies are blood protein produced in response to and counteracting a specific antigen. Antibodies combine chemically with substances which the body recognizes as alien, such as bacteria, viruses, and foreign substances in the blood.

They are produced by the body's B cells to fight infections like bacteria, viruses, and other invasive pathogens. When B cell recognizes a specific pathogen-derived "antigen" molecule, it can proliferate and develop into plasma cells that secrete large amounts of antibody capable of binding to the antigen and fending off the infection.

B cells need a second signal to start proliferating and developing into plasma cells. This second signal can be provided by short DNA fragments called CpG oligonucleotides, which activate a protein inside B cells called TLR9.

But treating patient-derived B cells with CpG oligonucleotides stimulates every B cell in the sample, not just the tiny fraction capable of producing a particular antibody.

Treating patient-derived B cells with tiny nanoparticles coated with both CpG oligonucleotides and the appropriate antigen. using this method, CpG oligonucleotides are only internalized into B cells that recognize the specific antigen, and these cells are therefore the only ones in which TLR9 is activated to induce their proliferation and development into antibody-secreting plasma cells.

 Some of the anti-influenza antibodies produced by the method recognized multiple strains of the virus and were able to neutralize its ability to infect cells.

The method does not depend on the donors having been previously exposed to any of these antigens through vaccination or infection; the researchers were able to generate anti-HIV antibodies from B cells isolated from HIV-positive patients.
Researchers generate therapeutic antibodies for the treatment of infectious diseases and cancer.
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Taking vitamin D in pregnancy protect babies from asthma

Taking vitamin D supplements in pregnancy strengthens babies' immune systems, which may lower their risk of developing asthma, new research reveals.

The unborn babies of expectant mothers who take more than the recommended daily vitamin D dose for pregnant women respond better when exposed to simulated pathogens.

Researchers from King's College London analysed the impact of taking a 4,400 IU vitamin D supplement every day during a woman's second and third trimester versus the recommended daily intake of 400 IU.

Study participants were randomised at 10 to 18 weeks of pregnancy to receive either high or low dose vitamin D.

The researchers then took umbilical cord blood samples from 51 pregnant women to assess the responsiveness of newborns' immune systems when exposed to simulated pathogens.

Results show that blood samples of babies born to mothers taking the higher vitamin D dose, had a greater immune response.





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