Research Roundup: T Helper Cells Post-COVID Vaccine Last At Least 6 Months and More

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Every week there are numerous scientific studies published. Here’s a look at some of the more interesting ones.

T Helper Cells Stay High 6 Months After COVID-19 Vaccination

Much of the news about waning immunity after COVID-19 vaccinations revolve around antibodies. Many immunologists have pointed out that memory T and B cells typically maintain efficacy to vaccines far longer than antibodies. A new study from Johns Hopkins Medicine confirms that theory. In a study of people who had received either the Pfizer-BioNTech or Moderna mRNA COVID-19 vaccines, they found persistently high CD4+ T lymphocytes, called helper T cells, six months after vaccination at only slightly decreased levels from after two weeks post-vaccination. These T cells recognize and help protect against the Delta variant as well.

“Previous research has suggested that humoral immune response — where the immune system circulates virus-neutralizing antibodies — can drop off at six months after vaccination, whereas our study indicates that cellular immunity — where the immune system directly attacks infected cells — remains strong,” said Joel Blankson, professor of medicine at the Johns Hopkins University School of Medicine and senior author of the study. “The persistence of these vaccine-elicited T cells, along with the fact that they’re active against the Delta variant, has important implications for guiding COVID vaccine development and determining the need for COVID boosters in the future.”

In the study, the number of helper T cells against SARS-COV-2 spike proteins was extremely low before vaccination, about 2.7 spot-forming units (SFUs) per million peripheral blood mononuclear cells (PBMCs). Between 7 and 14 days after vaccination, the frequency rose to 237 SFUs per million PBMCs. Six months after vaccination, it dropped slightly to a median of 122 SFUs per million PBMCs, still about sixty times higher than before vaccination. The research was published in the journal Clinical Infectious Diseases.

Newly Found Gene Contributes to Type 1 Diabetes Progression

Researchers with Augusta University found that a combination of pro-inflammatory receptors, CCR2 and its ligand, CCL-2, increased the risk of developing type 1 diabetes. Type 1 diabetes, formerly called juvenile diabetes, is an autoimmune disease where the immune system attacks the islet cells in the pancreas that produce insulin. It requires insulin treatment for the rest of the patient’s life. They identified the involvement of these receptors by studying the longitudinal data of 310 people enrolled in DAISY, a study funded by the National Institute of Health and the University of Colorado Anschutz Medical Campus (Aurora). The research was published in the Journal of Translational Autoimmunity.

Previously, CCR2 was not directly associated in humans with type 1 diabetes. However, it had been observed that in mice, when the gene was knocked out, they were less likely to develop diabetes. Broadly, in people, they know that higher CCR2 gene expression is likely to cause unwanted recruitment of immune cells, which is associated with other autoimmune diseases such as rheumatoid arthritis and multiple sclerosis. Their research supports the idea that inhibiting the CCR2 receptor might be a way to delay the progression of type 1 diabetes, even though trials of CCR2 inhibition have not been effective in rheumatoid arthritis and multiple sclerosis, potentially because the treatment started too late.

The authors wrote, “Our findings support the potential of CCR2 inhibition in delaying the progression of islet autoantibody-positive individuals to T1D. CCR2 inhibition could impair the recruitment of immune cells, including T cells and monocytes, to the pancreatic islet, and thus, delay the progression to islet autoimmunity. Several CCR2 inhibitors have been tested in clinical trials for cardiovascular disease, diabetic nephropathy, cancer, and autoimmunity.”

New Insights into Tau in ALS

Researchers at Massachusetts General Hospital found that people with amyotrophic lateral sclerosis (ALS) who carry a mutation in the C9orf72 gene had elevated levels of tau and phosphorylated tau in the motor cortex region of the brain. They also identified new mutations in the tau gene and found that the ratio of different forms of tau might be used as an indicator of ALS disease progression. They used post-mortem brain samples from ALS patients. Tau is a protein important for stabilizing the structure of nerve cells, but it has been implicated in Alzheimer’s disease. The researchers were trying to determine if it plays a role in ALS, because it often aggregates and leads to cellular dysfunction in Alzheimer’s and other neurodegenerative disorders. 

Altered Fat Metabolism Associated with ALS

Scientists with Johns Hopkins Medicine used genetically engineered mice and human cell and tissue samples to show that higher inflammatory chemical levels associated with fat metabolism are linked to amyotrophic lateral sclerosis (ALS). The research focused on genetic pathways tied to how spinal motor cells process fats. People with ALS had about 2.5-fold higher levels of arachidonic acid, a lipid typically seen in the fatty parts of meat and fish, and which are known to stimulate inflammatory processes. By decreasing the arachidonic acid pathway in mice models of ALS, the researchers decreased the disease’s muscle-weakening symptoms and extended the animals’ lives.

People on SSRI Antidepressants Less Likely to Die of COVID-19

A study out of the University of California – San Francisco found that people taking a class of antidepressants called selective serotonin reuptake inhibitors (SSRIs), especially fluoxetine, were significantly less likely to die of COVID-19 than people in a matched control group. The data was analyzed from health records from 87 centers across the U.S. The data was from almost 500,000 patients, including 83,584 adults diagnosed with COVID-19 between January and September 2020. Of those patients, 3,401 were prescribed SSRIs.

“We can’t tell if the drugs are causing these effects, but the statistical analysis is showing significant association,” said Marina Sirota, associate professor of pediatrics and a member of the Bakar Computational Health Sciences Institute (BCHSI) at UCSF. “There’s power in the numbers.”

The research found that patients taking fluoxetine (sold under the brand names Prozac and Sarafem) were 28% less likely to die of COVID-19, and patients taking either fluoxetine or fluvoxamine (brand names Luvox, Faverin, Fluvoxin) were 26% less likely to die. Out of the entire group, patients taking any kind of SSRI were 8% less likely to die of COVID-19 than the matched patient control group. Other common brands of SSRIs include Celexa (citalopram), Lexapro (escitalopram), Paxil (paroxetine) and Zoloft (sertraline).

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