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Immune reaction


Wednesday 15/09/2021

Researchers from UZ Gent and VIB (Flemish Institute for Biotechnology) have studied the production of COVID-19 antibodies in the nose. 78.3% of the study participants built up antibodies at that site after their vaccination. Those antibodies in the nose can be a major brake on infection and spread.


'The coronavirus enters our body through the upper respiratory tract,' explains nose, throat and ear specialist Prof. Philippe Gevaert. ' Neutralizing antibodies in our blood render the virus harmless by blocking the binding of the spike proteins to human cells. If the antibodies are also present in the nose, they can already form a first barrier there against the entry of the virus. It is therefore important to also investigate the reaction to an infection and vaccination in the nose.'



  1. The blood and nose were examined twice in 46 study participants: just before the first vaccination with Pfizer or AstraZeneca and 13 to 40 days after the second vaccination. 23 participants had an infection before their vaccination. Just before their first vaccination , only 17.4% of them showed antibodies in the nose .
  2. After full vaccination , 78.3% of all participants built up antibodies in the nose. The participants who received Pfizer showed more antibodies (96%) than the participants who received AstraZeneca (59%). Also, the local antibodies in Pfizer showed a stronger neutralization of the viral spike protein than in AstraZeneca. A past COVID-19 infection had no influence on the results.
  3. The blood analysis showed the same amount of antibodies in both vaccination groups.

It is not yet clear why one vaccine elicits antibodies in the nose more often than another. 'The explanation may lie in a different time span between the two doses or in a different effect of the vaccines,' suspects infectious disease specialist Prof. Dr. Linos Vandekerckhove. 'During a follow-up study , we will map the further evolution of the antibody response in the blood and in the nose. We hope to get more clarity this way.'






  • Discovery could prevent development of brain tumors in children. Developmental Cell, Oct 2014.
    A mechanism that promotes the progression of medulloblastoma, the most common brain tumour found in children, has been discovered. The team found that the protein Boc, required for Sonic Hedgehog to induce DNA damage, causes the cancer to develop.
  • Finding new genetic links to prostate cancerNature Genetics, Sept 2014.
    23 new regions of the genome have been discovered that influence the risk for developing prostate cancer. This study brings the number of genetic variants linked to prostate cancer to 100. Testing for those variants can identify men with a risk of the disease that is almost six times higher than average.
  • Early sign of pancreatic cancer identified by researchers. Nature Medicine, Sept 2014.
    A sign of the early development of pancreatic cancer has been identified. It is an upsurge in circulating branched-chain amino acids that occurs before the disease is diagnosed and symptoms appear.
  • Modified vitamin D shows promise as treatment for pancreatic cancer. Cell, Sept 2014.
    A synthetic derivative of vitamin D was found to collapse the barrier of cells shielding pancreatic tumors, making this seemingly impenetrable cancer much more susceptible to therapeutic drugs. Vitamin D has been tried multiple times as a therapy for pancreatic cancer and never worked, since activated stellate cells in pancreas rapidly break down normal vitamin D, preventing the vitamin from binding to the receptor. But systematic analysis of vitamin D analogues allowed the team to discover a modified form of vitamin D that is more stable, resilient and effective…
  • Genome-wide association study identifies multiple susceptibility loci for pancreatic cancerNature Genetics, Aug 2014.
    a genome-wide association study (GWAS) of people with and without pancreatic cancer has identified several new genetic markers that signal increased risk of developing the highly lethal disease. The discovery of these markers is important for several reasons. One is that further study of these DNA variants may help explain on the molecular level why some people are more or less susceptible to pancreatic cancer than the average person. A second is the potential to identify people at increased risk who then might be candidates to undergo MRI or ultrasound scanning to look for early, treatable pancreatic tumors.
  • Targeting mTOR dependency in pancreatic cancerGut, Aug 2014.
    Rapamycin shrinks a particular type of pancreatic cancer (caused by PTEN mutation) and stops it spreading. Previous clinical trials did not find this drug to be effective as a treatment for pancreatic cancers when it was given to all patients with different forms of the disease. Since one in five carried a faulty PTEN gene, this gives hope that a substantial number of patients could benefit from treatment with rapamycin.
  • Repurposing anti-depressant medication to target medulloblastomaNature Medicine, Aug 2014.
    A novel molecular pathway that causes an aggressive form of medulloblastoma has been identified.
  • Potential way to halt pancreatic cancer spread. Gastroenterology, May 2014.
    Switching off a key protein ‘fascin’ in pancreatic cells slows the spread of the disease to other tissues.
  • Genetic test could improve colon cancer screeningNew England Journal of Medicine, March 2014.
    A non-invasive test that includes detection of the genetic abnormalities related to cancer could significantly improve the effectiveness of colon cancer screening.
  • New hormone receptors discovered to target when treating breast cancerJournal of Clinical Investigation, Feb 2014.
    There are other receptors in breast cancer that can be targeted — androgen and vitamin D receptors. Since at least 50 percent of patients with breast cancer express all three receptors — estrogen, androgen and vitamin D in their tumor cells, this may allow clinicians to consider triple hormone treatments, which is a new concept, as opposed to treating patients by targeting only estrogen receptors.

  • Immune Cells and Virus Team Up to Fight Cancer. Science Translational Medicine, 5 March 2014.
    The findings demonstrate that localized therapy with oncolytic NDV induces inflammatory immune infiltrates in distant tumors, making them susceptible to systemic therapy with immunomodulatory antibodies, which provides a strong rationale for investigation of such combination therapies in the clinic.
  • Cancer vaccine could use immune system to fight tumors. Gene Therapy, February 27, 2014.
    IL-15 is a powerful pro-inflammatory protein that can enhance immune responses. Recently, human Interleukin-15 (IL-15) has entered clinical trials for treatment of patients with melanoma and renal cancer. In this study, genetically modified tumor cells producing IL-15 and IL-15Ra induced anti-cancer responses.

  • New leukemia immune cell therapy shows promise. Science Translational Medicine, 19 February 2014.
    In the latest and largest clinical study yet conducted in patients with advanced leukemia, 14 of the 16 patients – that is 88% – treated with genetically modified versions of their own immune cells, achieved complete remission, at least in the short term.

  • The PRKC1 and SOX2 Oncogenes Are Coamplified and Cooperate to Activate Hedgehog Signaling in Lung Squamous Cell Carcinoma. Cancer Cell, 10 February 2014.
    PKC1 and SOX2 are genetically, biochemically, and functionally linked in LSCC, and together they drive tumorigenesis by establishing a cell-autonomous Hh signaling axis.

  • UHRF1 Overexpression Drives DNA Hypomethylation and Hepatocellular Carcinoma. Cancer Cell, 30 January 2014.
    Overexpression of UHRF1, a critical DNA methylation regulator, in zebrafish causes DNA hypomethylation, p53-mediated senescence, and hepatocellular carcinoma (HCC) when senescence is bypassed. UHRF1 overexpression is a mechanism underlying DNA hypomethylation in cancer cells and that senescence is a primary means of restricting tumorigenesis due to epigenetic disruption.

  • Engineered virus effective against triple negative breast cancer cells. The FASEB Journal, January 30, 2014.
    Cancer gene therapy through vaccinia virus which infected cancer cells and produced a cell surface protein called hNIS that normally is used to concentrate iodine in thyroid cells. This discovery combines proven cures (this virus and radioactive iodine) for two other diseases, presenting a potential cure for one of the most aggressive and least treatable forms of breast cancer called “triple negative breast cancer.”

  • New breast cancer stem cell findings explain how cancer spreads. Stem Cell Reports, 14 January 2014.
    Breast cancer stem cells exist in two different states (the epithelial-mesenchymal transition (EMT) state and the mesenchymal-epithelial transition (MET) state) and each state plays a role in how cancer spreads. The finding sheds new light on the process that makes cancer a deadly disease: “You need both forms of cancer stem cells to metastasize and grow in distant organs. If the stem cell is locked in one or the other state, it can’t form a metastasis,” The author Dr. Wicha says.

  • Immune cells engineered to express interferon-a halt breast tumor formation and metastasis. Science Translational Medicine, January 1, 2014.
    Genetic Engineering of Hematopoiesis for Targeted IFN-a Delivery Inhibits Breast Cancer Progression. This study validated the feasibility, safety, and therapeutic potential of a new cancer gene therapy strategy, and opened the way to test this approach as adjuvant therapy in advanced breast cancer patients.

  • Molecular Engines Star in New Model of DNA Repair. Nature, January 16, 2014.
    How an enzyme called RNA polymerase patrols the genome for DNA damage and helps recruit partners to repair it. The result: fewer mutations and consequently less cancer and other kinds of disease.
    Damaged DNA lesions that result from exposure to ultraviolet light interfere with transcription, causing RNA polymerase to stall. UvrD, a DNA helicase required for nucleotide excision repair, can remove such lesions, but its exact role was unknown. Evgeny Nudler and colleagues now show that UvrD is a transcription elongation factor that binds RNA polymerase and promotes its backwards movement when it becomes stalled at a lesion. NusA, another elongation factor, assists in promoting backtracking and helps UvrD to target other nucleotide excision repair factors to the exposed lesion.

  • Silencing HoxA1 by Intraductal Injection of siRNA Lipidoid Nanoparticles Prevents Mammary Tumor Progression in Mice. Science Translational Medicine, January 1, 2014.
    This approach that leverages new advances in systems biology and nanotechnology offers a novel noninvasive strategy to block breast cancer progression through targeted silencing of critical genes directly within the mammary epithelium.



  • Altering Community of Gut Bacteria Promotes Health and Increases Lifespan. Cell, January 12, 2014.
    Study provides first systemic understanding of aging gut. Having the right balance of gut bacteria may be the key to enjoying a long healthy life. Scientists promoted health and increased lifespan in Drosophila by altering the symbiotic relationship between bacteria and the absorptive cells lining the intestine. The work provides a model for studying diseases associated with the aging gut, and how we go from having a young, healthy gut to one that is old and decrepit……Jasper said the most exciting result of their study occurred when his group increased the expression of PGRP-SC in epithelial cells of the gut, which restored the microbial balance and limited stem cell proliferation. This enhancement of PGRP-SC function, which could be mimicked by drugs, was sufficient to increase lifespan of flies. “If we can understand how aging affects our commensal population – first in the fly and then in humans – our data suggest that we should be able to impact health span and life span quite strongly, because it is the management of the commensal population that is critical to the health of the organism.”


Alzheimer’s disease

  • Reelin protein rescues cognitive deficits in an animal model of Alzheimer’s disease. Nature Communications, March 6, 2014.
    Reelin, a crucial protein for adult brain plasticity, recovers cognitive functions in mice with Alzheimer’s disease. This new preclinical study demonstrates that an increase in Reelin brain levels avoids cognitive deterioration in mouse models of Alzheimer’s disease. Moreover, Reelin delays amyloid-beta fibril formation in vitro and reduces amyloid deposits in mice with Alzheimer’s.

  • Longitudinal Change in CSF Biomarkers in Autosomal-Dominant Alzheimer’s Disease. Sci Transl Med 5 March 2014.
    These results emphasize the importance of longitudinal, within-person assessment when modeling biomarker trajectories across the course of the disease.

  • Alzheimer’s disease much larger cause of death than reported. Neurology, March 5, 2014.
    Alzheimer’s disease may contribute to close to as many deaths in the United States as heart disease or cancer.

  • Blood test predicts Alzheimer’s. Nature Medicine, March 09, 2014
    Researchers discovered a blood test that can predict with 90% accuracy if a healthy person age 70 or older will develop mild cognitive impairment or Alzheimer’s disease over a three-year period. This is a major step toward the commercialization of a preclinical disease biomarker test that could be useful for large-scale screening to identify at-risk individuals.

  • Raising SORLA activity could protect from Aβ peptide accumulation. Science Translational Medicine, 12 February 2014.
    SORLA is a sorting receptor genetically associated with both sporadic and familial forms of AD. Its new function is to direct newly produced Aβ to lysosomes for degradation. This study substantiates the beneficial effects of raising SORLA activity for AD-related processes, and identifies lysosomal sorting of Aβ as a new pathway that may be amenable to therapeutic intervention.

  • New findings suggest benefit of vitamin E in mild to moderate Alzheimer’s disease by slowing functional decline. JAMA. January 1, 2014.
    This change in the alpha tocopherol (a form of vitamin E that is preferentially absorbed and accumulated in humans) group translates into a delay in clinical progression of 19% per year compared with placebo or a delay of approximately 6.2 months over the mean follow-up of 2.27 years. In patients with moderately severe Alzheimer’s disease, alpha tocopherol (2000 IU/d) was shown to be effective in slowing clinical progression.



  • High-Fiber Diet May Ward Off Asthma. Nature Medicine, 05 January 2014.
    The fiber consumed in fruits and vegetables seems to help quiet the overzealous immune system activity that leads to such conditions as irritable bowel syndrome, Crohn’s disease, and possibly even colon cancer. Now it appears that a diet rich in fiber may also fend off asthma. This study is the first to show that diet can influence the production of immune cells in the bone marrow, which could have major implications given that immune cell precursors leave the bone marrow and spread to tissues throughout the body, including the lung. Medium report.


Diabetes and Obesity

  • FDA Approved Contrave, 3rd Weight-Loss Pill in recent two years
    Other drugs in the same category include Qsymia and Belviq. All the recently approved drugs focus on reducing appetite and none of the drug assures about massive weight loss.
  • Leptin also influences brain glial cells to control appetite. Nature Neuroscience, June 1, 2014
    Twenty years after the hormone leptin was found to regulate metabolism, appetite, and weight through brain cells called neurons, researchers have found that the hormone also acts on other types of cells, glial cells, which provide the main barrier between the periphery and the brain, and therefore could be targeted for drugs that treat metabolic disorders, including obesity and diabetes.
  • Obesity rates climbing worldwide. The Lancet, May 28, 2014
    Worldwide, there has been a startling increase in rates of obesity and overweight in both adults (28% increase) and children (up by 47%) in the past 33 years, with the number of overweight and obese people rising from 857 million in 1980 to 2.1 billion in 2013, according to a most comprehensive global study to date.
  • Clinical trial reaffirms diet beverages play positive role in weight lossObesity, May 27, 2014
    This study clearly demonstrates that diet beverages can in fact help people lose weight, directly countering myths in recent years that suggest the opposite effect — weight gain.
  • Muscle Molecule (ß-aminoisobutyric acid) After Exercise Spurs Fat Cells to Slim Down, Discovery could lead to drugs to fight obesity, diabetes. Cell Metabolism, 7 January 2014.
    Exercise stimulates muscles to release a molecule: ß-aminoisobutyric acid (BAIBA), which induces white fat cells to become more like brown fat cells, altering their gene activity patterns. And it stimulates other cell types, stoking fat metabolism in the liver. Medium report. 
  • New Obesity Guidelines: Promise and Potential. JAMA. January 2014.
  • Sugar intake not directly related to liver diseaseGastroenterology, November 1, 2013
    Despite current beliefs, sugar intake is not directly associated with nonalcoholic fatty liver disease, according to a new study. Rather, high-calorie diets promote the progression of this serious form of liver disease.
  • How diabetes drug delays aging in worms. CELL. March 28, 2013
    A widely prescribed type 2 diabetes drug, Metformin, slows down the aging process by mimicking the effects of dieting, according to a study using worms to investigate how the drug works.


  • Distribution, recognition and regulation of non-CpG methylation in the adult mammalian brain. Nature Neuroscience 17,215–222(2014)
    Non-CpG methylation has been found in stem cells, and in neurons in the brain, acting as a system of gene regulation, which can be independent of traditional CpG methylation and may play more of a role in managing operations in mature cells.



  • Strategies for developing new antiviral flu drugs. Virology, April 2014.
    New analysis of the influenza A virus shows potential for developing new anti-viral drugs which are more likely to be universally effective against the flu virus originating from avian, swine or human virus strains.
  • Three quarters of people with seasonal, pandemic flu have no symptoms. The Lancet Respiratory Medicine, March 17, 2014
    Around 1 in 5 of the population were infected in both recent outbreaks of seasonal flu and the 2009 H1N1 influenza pandemic, but just 23% of these infections caused symptoms, and only 17% of people were ill enough to consult their doctor.
  • An autoreactive antibody from an SLE/HIV-1 individual broadly neutralizes HIV-1. J Clin Invest. March 10, 2014
    One person having a rare combination of both lupus and HIV, has the unique ability to fight HIV. This provided key insights into an immune response that researchers now hope to trigger with a vaccine, according to new findings.

  • Seasonal flu vaccine may cut stroke risk. Vaccine, March 10, 2014
    patients who had been vaccinated against influenza were 24% less likely to suffer a stroke in the same flu season-an added health benefit.

  • Gene Editing of CCR5 in Autologous CD4 T Cells of Persons Infected with HIV. N Engl J Med, March 6, 2014
    The immune cells of 12 HIV positive patients have been successfully genetically engineered by researchers to resist infection, and decrease the viral loads of some patients taken off antiretroviral drug therapy (ADT) entirely -— including one patient whose levels became undetectable. This it the first published report of any gene editing approach in humans.

  • HPV vaccine provides significant protection against cervical abnormalities. BMJ, March 4, 2014
    The data concludes a risk reduction of 46% for confirmed high grade cervical abnormalities and 34% for other cervical abnormalities for young women who were fully vaccinated with the HPV vaccine prior to their first smear test.

  • Potent HIV antibody research has opened up possibilities for HIV prevention, treatment. Nature, March 3, 2014.
    A KwaZulu-Natal woman’s body responded to her HIV infection by making potent antibodies (called broadly neutralizing antibodies, because they are able to kill multiple strains of HIV from across the world). Researchers identified these antibodies in her blood and then duplicated them by cloning the antibodies in the laboratory. The cloned antibodies were then used in a series of experiments in the laboratory to elucidate the pathway followed by her immune system to make these potent antibodies.

  • Light zaps viruses: How photosensitization can stop viruses from infecting cells. J. Virol. February 2014.
    Photosensitizing a virus’s membrane covering can inhibit its ability to enter cells and potentially lead to the development of stronger, cheaper medications to fight a host of tough viruses.

  • Breast cancer drug Tamoxifen fights fungal disease. mBio, February 11, 2014
    Tamoxifen, a drug currently used to treat breast cancer, also kills a fungus that causes a deadly brain infection in immunocompromised patients. The findings could lead to new treatments for a disease that kills more HIV/AIDS patients than tuberculosis.

  • Geranium extracts inhibit HIV-1. PLoS One. January 29, 2014.
    Extracts of the geranium plant Pelargonium sidoides inactivate human immunodeficiency virus type 1 (HIV-1) and prevent the virus from invading human cells. Scientists report that these extracts represent a potential new class of anti-HIV-1 agents for the treatment of AIDS.

  • Vitamin A may help boost immune system to fight tuberculosis. The Journal of Immunology, February 25, 2014 The UCLA team describes for the first time the mechanism by which vitamin A and its downstream gene NPC2 assist the immune system by reducing the level of cholesterol in cells infected with TB.
  • Promising class of antibiotics discovered for treatment of drug-resistant tuberculosis. Nature Medicine, January 27, 2014
    The antibiotics, called spectinamides, were created by changing the chemical structure of an existing antibiotic, spectinomycin, which does not work against TB.



  • 2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults. JAMA. December 18, 2013 


Parkinson’s disease

  • Nerve growth factor halts mitochondrial degeneration. EMBO J. 03 February 2014. The PINK1 gene plays a role in Parkinson’s disease, whose mutation causes mitochondrial dysfunction. The activation of the Ret receptor, which binds the growth factor GNDF in humans, counteracts this degeneration. This important new link could lead to the development of more refined GDNF therapies.



  • Stem cells overcome damage in other cells by exporting mitochondria. The EMBO Journal, January 16, 2014.
    A research team has identified the protein Miro1 that increases the transfer of mitochondria from mesenchymal stem cells to lung cells. The researchers reveal that the delivery of mitochondria to human lung cells can rejuvenate damaged cells. The migration of mitochondria from stem cells to epithelial cells also helps to repair tissue damage and inflammation linked to asthma-like symptoms in mice.
  • Gene makes old cells act young again. Cell. 2013 Nov 7;155(4):778-92.
    Turning on a gene called Lin28a in old tissue may help cells heal like they are young again. Reactivating Lin28a, along with other techniques, could help adult humans heal more quickly after an injury.