A groundbreaking new study by UC Davis researchers has uncovered why obesity both fuels cancer growth and allows blockbuster new immunotherapies to work better against those same tumors.
Scientists at the University of Liverpool have discovered a new and important function of a toxin produced by disease-causing bacteria that could have significant implications for future vaccine design.
Nearly two thirds of Americans (65 percent) say antibiotic resistance is a public health problem and a strong majority (81 percent) say they are concerned that antibiotic resistance will make more infections difficult or impossible to treat and even deadly, according to a national public opinion survey commissioned by Research!America in collaboration with the Infectious Disease Society of America (IDSA).
Immune cells called Gamma Delta T cells can act independently to identify and kill cancer cells, defying the conventional view of the immune system. This will help scientists to understand and treat cancer and autoimmune conditions such as inflammatory bowel disease.
Vaccinia virus, a poxvirus closely related to smallpox and monkeypox, tricks cells it has infected into activating their own cell movement mechanism to rapidly spread the virus in cells and mice, according to a new UCL-led study published in Nature Microbiology.
The body's immune surveillance systems stutter and fail in the presence of excess fat, which reduces their ability to fight cancer and disease. The results highlight immuno-metabolic pathways as a promising target to reverse immune defects in obesity, and suggest that metabolic reprogramming of Natural Killer cells may kick-start their anti-cancer activity and improve treatment outcomes.
The mechanisms that trigger the elimination of T cells that pose autoimmune dangers work very mechanically via physical forces. T cell precursors must loosen their grip on human antigens within a reasonable time in order to advance to being T cells and defend the body. But if precursor T cells, thymocytes, grip the human antigens too tightly, the immune cells must die. Here's how the grip of death works.
An experimental drug may be effective against a deadly form of pancreatic cancer when used in combination with other immune-boosting therapies, according to a cover study publishing online Nov. 12 in Cancer Cell.
A research team from Massachusetts Eye and Ear describes a newly discovered mechanism in a report published in the Journal of Allergy and Clinical Immunology (JACI). The findings shed new light on our immune systems -- and also pave the way for drug delivery techniques to be developed that harness this natural transportation process from one group of cells to another.
Patients with X-linked lymphoproliferative syndrome type 1 (XLP1) are at risk of fatal infectious mononucleosis. Here, a Tokyo Medical and Dental University (TMDU)-led research team performed detailed analyses of T cells in a family with a mild form of XLP1. They found small populations of CD4+ and CD8+ T cells expressing SLAM-associated protein at normal levels, suggesting that less invasive therapies, which affect fewer T cells, may be useful in treatment of XLP1.