Jatin Sharma - Department of Infectious Disease
Link: https://doi.org/10.1126/science.ade9733
The article, “Infection infidelities drive innate immunity” by Jonathan C. Kagan, a gastroenterologist at Harvard Medical School, discusses the revolutionary thesis that human immune cells don’t directly respond to bacterial and viral pathogens themselves, but rather respond to mistakes made by unsuccessful pathogens. When pathogens make errors- like replication mistakes or mutations that lead to their own death (unsuccessful pathogens) - they release specific patterns that our immune cells can detect. Kagan’s thesis emphasizes how successful pathogens, on the other hand, escape detection by the immune system. This concept challenges the conventional understanding of how the human immune system detects pathogens, which is by focusing on all pathogens, regardless of their success. Kagan’s hypothesis has gained significant attention and positive feedback from the scientific community, with many researchers providing additional examples to support the idea that errors made by pathogens play a crucial role in driving our immune response.
If immune cells do indeed respond to pathogen errors, it opens up new opportunities for developing immunotherapy; like in cancer treatments done by activating the immune system to better recognize and attack cancer cells. By targeting and exploiting unsuccessful pathogens, researchers could potentially enhance the immune response against pathogens that have evolved mechanisms to evade detection. Treatments could be designed to specifically induce or enhance mistakes/errors by pathogens,allowing for better detection by immune cells and a stronger immune response. This could be achieved through the use of targeted drugs or modifications that promote higher mutation rates and interfere with the pathogen's replication. If Kagan’s thesis is true, it could revolutionize treatments for infectious diseases and cancers.
References:
Kagan, J. C. (2023). Infection infidelities drive innate immunity. Science, 379(6630), 333–335. https://doi.org/10.1126/science.ade9733
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