The study reveals that moderate fever enhances CD4 T cell activity while reducing regulatory T cell suppression, highlighting temperature's immune effects.
By Pooja Toshniwal PahariaReviewed by Danielle Ellis, B.Sc.Sep 25 2024 Study reveals that moderate fever temperatures improve metabolism, proliferation, and effector function of CD4 T cells while reducing regulatory T cell suppression.
Fever occurs when the body's thermostat, located in the hypothalamus, raises the set-point temperature in response to infection, inflammation, or other causes. Symptoms include sweating, chills, headache, muscle aches, and fatigue. Researchers cultured murine helper T cells at 37°C or 39°C to examine T-cell changes caused by temperature elevation. Ki67 expression in the spleen and mesenteric lymph nodes indicated T-cell proliferation, whereas interferon-gamma levels indicated their function. Phosphorylated protein kinase B -mammalian target of the rapamycin C1 pathway components represented T-cell metabolism. Enzyme-linked immunosorbent assays measured cytokine expression.
Related StoriesResearchers used in vitro Clustered Regularly Interspaced Short Palindromic Repeats screening among Th1 cells to determine the molecular basis of cell death. They extracted T cells from wild-type and Trp53−/− mice and cultured them at 37° and 39°C to assess their viability. The researchers conducted gene expression studies in mice with inflammatory bowel disease to investigate whether in vivo inflammation produced comparable stress responses as functional correlations.
The heat affects ETC1 and increases oxidative stress in the mitochondria, or energy-producing components of a cell. This lowers cell viability and damages the DNA. The increased stress and DNA damage cause apoptosis or programmed cell death. In this situation, several murine and human Th1 cells, a type of helper T cell, are destroyed.
Heat Arthritis CD4 Cell Cell Death Cell Metabolism Chronic CRISPR DNA DNA Damage Fatigue Genes Glycolysis Headache Hypothalamus Immunology Inflammation Interferon Metabolism Mitochondria Muscle Oxygen Proliferation Protein Respiratory Rheumatoid Arthritis Stress T-Cell
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