Communication, serendipity, and a histone modifier enzyme called DOT1L (disruptor of telomeric silencing 1-like) have all combined to produce some exciting findings on the immune system's B cells and T cells by two groups of Monash Biomedicine Discovery Institute (BDI) (Australia) scientists. The new results could result in further studies into a target for asthma and allergies, and fundamental work exploring the formation of immunity itself. Two papers on DOT1L by teams led by BDI’s Professor Colby Zaph and Associate Professor Kim Good-Jacobson--whose labs are next door to each other--were both published online on December 16, 2020 in Cell Reports. Dr. Zaph’s article is titled “The Methyltransferase DOT1L Controls Activation and Lineage Integrity in CD4+ T Cells During Infection and Inflammation" (https://www.cell.com/cell-reports/pdf/S2211-1247(20)31494-7.pdf). Dr. Good-Jacobson’s article is titled “The Histone Methyltransferase DOT1L Is Essential for Humoral Immune Responses” (https://www.cell.com/cell-reports/pdf/S2211-1247(20)31493-5.pdf). Professor Zaph and colleagues found that the DOT1L enzyme was critical in controlling how T cells (white blood cells critical for immunity to infections) (image) make the choice to develop into distinct subsets. T cells have the ability to adopt a variety of fates that depend on the type of infection they face. Type 1 T cells (Th1) for example are critical for clearing viral infections, while type 2 T cells (Th2) are required for immunity to worm parasites. Critically, dysregulated Th1 cells can cause diseases such as inflammatory bowel disease, diabetes, and arthritis, and uncontrolled Th2 cell responses can lead to asthma and allergies.
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