2024-01-13 07:00:02
A 25-year-old cellular puzzle has been solved, revealing that cellular cannibalism may be the cause of a rare human immunodeficiency. This discovery, emanating from studies on fruit flies, mice and humans, opens new perspectives for an innovative treatment once morest cancer.
The central point of this research is the embarrassed Rac2. Rac proteins are essential for the formation of the cellular cytoskeleton, allowing cell movement and shape. Denise Montell,University of California in Santa Barbara, first discovered their importance by studying the ovaries of flies fruit. She observed that a hyperactive form of protein Rac1 might destroy All ovarian tissue.
The study then established a link with cellular cannibalism, a phenomenon frequently observed in normal fly egg development. The researchers found that Rac2 played a key role in this process, helping cells engulf their neighbors.
Meanwhile, a study published in Blood showed that people with recurrent infections shared a mutation that excessively activated Rac2, leading to a significant loss of T cells. These results led to the hypothesis that active immune cells, such as neutrophils , might consume T cells, similar to the phenomenon observed in fruit flies.
Many aspects of the immune system are implicated in these findings.
Credit: Matt Perko, UC Santa Barbara
The therapeutic implications of this discovery are considerable. Meghan Morrissey proposed a method, called CAR-M, of programming macrophages to destroy cancer cells. The addition of activated Rac2 might strengthen this approach, as demonstrated by the work of Denise Montell’s team.
This research raises fundamental and practical questions, particularly on the application of this technique in the treatment of cancer in humans. Researchers are now exploring the effectiveness of this method in animal and human models, paving the way for potential new cancer therapies.
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