01
The gut mycobiota is recognized as crucial for intestinal homeostasis and immune function, yet the variability in fungal colonization of laboratory mice has complicated studies on the evolutionary and immune processes underlying commensalism. This research aims to address the gap by identifying a natural mouse gut symbiont and examining its effects on the host's immune system.
This study identified Kazachstania pintolopesii as a prominent fungal symbiont in wild mice that can significantly influence the gut mycobiome and immune responses. The researchers found that K. pintolopesii has an exceptional ability to colonize the gastrointestinal tract of mice, doing so in a bacteria-independent manner and leading to enhanced resistance against other fungi. This colonization is shielded from host immune surveillance, allowing the fungus to persist as a commensal. The study further revealed K. pintolopesii's ability to trigger a type 2 immune response under changing mucosal conditions, specifically through the induction of epithelial IL-33 and the IL-33–ST2 signaling pathway, which leads to gastrointestinal eosinophilia. The research also examined the context-dependent effects of K. pintolopesii on host resistance to helminth infections and the exacerbation of gastrointestinal allergies. Mechanistically, the study determined that K. pintolopesii activates type 2 immunity during mucus fluctuations, which has implications for understanding mucosal immunology and host-microbiota interactions. The findings provide a foundation for further exploration of the role of fungal commensals in health and disease.
They conclude that K. pintolopesii is a significant mouse commensal that can influence experimental outcomes and phenotypes, emphasizing the need to account for its presence in mouse facilities. It serves as a model for studying gut fungal commensalism and immunity, highlighting the complex interplay between host and symbiont in shaping immune responses.
DOI: 10.1038/s41586-024-08213-2
02
This study explores the role of Group 2 Innate Lymphoid Cells (ILC2s) in the development and function of B1 cells, a type of white blood cell crucial for the immune response. There has been a debate on whether ILC2s are essential for the type 2 immune response or if their function can be compensated by other cells, such as T cells.
The researchers found that B1 cells do not develop properly in the absence of ILC2s, indicating a non-redundant role for ILC2s. They demonstrated that the IL-33 receptor on ILC2s is an essential regulator of IL-5 production, which is vital for B1 cell development. The study also showed that conditional deletion of Il5 in ILC2s leads to defective B1 cell development and immunoglobulin production. This finding was further supported by the observation that B1 cells with specific B cell receptor rearrangements were reduced in ILC2-deficient mice.
They conclude that ILC2s are indispensable for the development of B1 cells and antibody production at barrier surfaces. The study establishes ILC2s as a non-redundant source of IL-5 required for B1 cell development, a function that cannot be compensated by other cell types, such as T cells. This discovery has significant implications for understanding the multilayered organization of the innate and adaptive immune system.
DOI: 10.1038/s41467-024-54780-3
关注我们获取更多免疫学文献资讯
Editor & Reviewer: Yanwen Zhu
