Western diets high in sugars reduce the number of Th17 inflammatory cells in the guts of mice, setting off a chain of events that lead to metabolic diseases, prediabetes, and obesity.
Organ-on-a-chip models reveal how different tissue contribute to inflammatory diseases such as ulcerative colitis.
Reducing dietary levels of methionine can slow the onset and progression of inflammatory and autoimmune diseases, such as multiple sclerosis, in those with high-risk factors.
Two studies reveal the role bile acids play in immunity and inflammation.
TH17 cells produced increased amounts of SerpinB1, a protein implicated in multiple sclerosis symptoms. SerpinB1 cells were identified with antibodies targeting the CXCR6 surface protein. Using monoclonal antibodies to target CXCR6, the cells disappeared significantly, and the mice primed to develop MS did not develop the disease.
A new PNAS study reveals why men are less likely to develop multiple sclerosis than women. According to researchers, a 'guardian molecule' that is triggered by testosterone appears to have a protective effect in men. When female mice were treated with the molecule, their symptoms of the disease were eliminated.
Researchers reveal high salt intake reduces resting cerebral blood flow and can contribute to dementia in mice.
Researchers have discovered how TH1 and TH17 immune cells obtain access to neurons in multiple sclerosis.
MIT researchers report mothers who contract severe infections during pregnancy face higher autism risks in their children. However, ASD risks could be reduced by blocking the function of certain strains of bacteria found in the mother's gut.
A new study reports researchers have been successful in protecting against the onset of multiple sclerosis in an animal model of the disease.
A new study identifies a possible genetic mechanism that causes a quicker progression of multiple sclerosis. The absence of Tob1 in CD4+ T cells is key to early onset of a more aggressive form of MS.
Gut bacteria, previously considered benign, has the ability to alter the immune system of mice enough to affect the rate of Multiple Sclerosis occurance.
