Microglia keep the Toxoplasma gondii parasite in check in the brain. Microglia release an immune molecule that recruit immune cells from the blood to control the parasite.
Study identifies the TLR7 gene as an essential player in the immune response against coronavirus infection.
Spinal cord injuries cause stem cells in the bone marrow to rapidly divide. Following the cell division, the stem cells become trapped in the bone marrow.
Findings suggest increased inflammation causes the aging process to accelerate, and there is a fine balance between maintaining immune system function and longevity.
Microglia help limit infection to the olfactory bulb and protects neurons from damage that could occur as a result of viral infection.
While the amount of antibodies generated varies widely in patients who have recovered from coronavirus, most people generate at least some antibodies which are intrinsically capable of neutralizing the SARS-CoV-2 virus.
After natural killer immune cells kill virus-infected cells, T and B immune cells produce cytokines. This makes the immune reaction stronger and results in the cytokine storm associated with severe COVID-19 infection.
SARS-CoV-2, the virus responsible for COVID-19, enters human cells by attaching to ACE2 and utilizing TMPRSS2. Drugs that block ACE2 or inhibit the enzyme could help treat the coronavirus, but only during early infection. As the infection progresses, SARS-CoV-2 becomes engulfed in human cells, reducing the number of ACE2 receptors on a cell and leading to an increase of angiotensin II in the blood. Angiotensin II triggers an inflammatory pathway, providing a positive feedback cycle, named IL-6 amplifier, resulting in excessive immune activation and the cytokine storm associated with severe COVID-19.
S309, a neutralizing antibody first identified in blood samples from a patient who recovered from SARS in 2003, shows promise for the treatment of COVID-19.