Poster Presentation CD1-MR1 2024

MAIT cells confer protective immunity against Aspergillus fumigatus in immunodeficient mice (#214)

Yuchen Zhou 1 2 , Huimeng Wang 1 3 , Bingjie Wang 1 2 , Yilu Huang 1 , Harshini Weerasinghe 4 , Adam Nelson 1 , Lucy Meehan 1 , Troi Pediongco 1 , Bronwyn Meehan 1 , Jeffrey Mak 5 6 , David Fairlie 5 6 , Alex Andrianopoulos 4 , Sidonia Eckle 1 , Zhongfang Wang 3 , James McCluskey 1 , Alexandra Corbett 1 , Zhenjun Chen 1
  1. Department of Microbiology and Immunology, University of Melbourne, Melbourne, VIC, Australia
  2. School of Medicine, Tsinghua University, Beijing, China
  3. State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong, China
  4. Genetics, Genomics and Systems Biology, School of BioSciences, University of Melbourne, Melbourne, VIC, Australia
  5. Division of Chemistry and Structural Biology, Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD, Australia
  6. Australian Research Council Centre of Excellence in Advanced Molecular Imaging, The University of Queensland, Brisbane, QLD, Australia

Mucosal-associated Invariant T (MAIT) cells recognise antigens that derive from microbial riboflavin biosynthesis, presented on Major Histocompatibility Complex Class I-related 1 (MR1). Research using mouse models has revealed the therapeutic potential of MAIT cells in combating bacteria that utilize the riboflavin biosynthesis pathway. However, the interplay between MAIT cells and fungi that synthesise riboflavin remains poorly understood. Aspergillus fumigatus, an important opportunistic human pathogen, has been shown in studies in vitro to be recognized and responded to by human MAIT cells.

To dissect the involvement of MAIT cells during A. fumigatus infection, we employed several mouse models, including both immunocompetent and immunodeficient strains. Our findings present evidence that A. fumigatus induces activation and expansion of MAIT cells in various organs, including the lungs (following pulmonary infection), livers, spleens, and peripheral blood (following systemic infection) in immunocompetent C57BL/6 mice, while their role in immune protection is not readily observable. In contrast, in settings where other immune cells are deficient, such as CD4 T cell-deficient GK1.5 transgenic mice, MAIT cell-associated protection could be observed, as evidenced by better fungal control post systematic infection in comparison to MAIT-deficient GK1.5.MR1-/- mice. Moving forward, we will delve into the mechanisms underlying the protective role of MAIT cells in such conditions.

In summary, our findings underscore a potentially important, albeit partially redundant, role for MAIT cells in providing immune protection against A. fumigatus and suggest that the manipulation of MAIT cells holds promise as a potential therapeutic avenue for severely immunodeficient patients with invasive Aspergillus infection.