@Article{biocell.2024.051383,
AUTHOR = {KERAN JIA, YANHAO ZHANG, MENGYU JIANG, MENGGE CUI, JIA WANG, JIAJIA ZHANG, HUIHAI ZHAO, MENGYAN LI, HUA WANG, QUANMING ZOU, HAO ZENG},
TITLE = {Single-cell transcriptomics reveals T-cell heterogeneity and immunomodulatory role of CD4<sup>+</sup> T native cells in <i>Candida albicans</i> infection},
JOURNAL = {BIOCELL},
VOLUME = {48},
YEAR = {2024},
NUMBER = {9},
PAGES = {1355--1368},
URL = {http://www.techscience.com/biocell/v48n9/57808},
ISSN = {1667-5746},
ABSTRACT = { <b>Objective:</b> <i>Candida albicans</i> is a common fungal pathogen that triggers complex host defense mechanisms,
including coordinated innate and adaptive immune responses, to neutralize invading fungi effectively. Exploring the
immune microenvironment has the potential to inform the development of therapeutic strategies for fungal
infections. <b>Methods:</b> The study analyzed individual immune cell profiles in peripheral blood mononuclear cells from
<i>Candida albicans</i>-infected mice and healthy control mice using single-cell transcriptomics, fluorescence quantitative
PCR, and Western blotting. We investigated intergroup differences in the dynamics of immune cell subpopulation
infiltration, pathway enrichment, and differentiation during <i>Candida albicans</i> infection. <b>Results: </b>Our findings
indicate that infiltration of CD4<sup>+</sup> naive cells, regulatory T (Treg) cells, and Microtubules (MT)-associated cells
increased after infection, along with impaired T cell activity. Notably, CD4<sup>+</sup> T cells and plasma cells were enhanced
after infection, suggesting that antibody production is dependent on T cells. In addition, we screened 6 hub genes,
transcription factor forkhead box protein 3(Foxp3), cytotoxic T-lymphocyte associated protein 4 (CTLA4),
Interleukin 2 Receptor Subunit Beta (Il2rb), Cd28, C-C Motif Chemokine Ligand 5 (Ccl5), and Cd27 for alterations
associated with CD4<sup>+</sup> T cell differentiation. <b>Conclusions:</b> These results provide a comprehensive immunological
landscape of the mechanisms of <i>Candida albicans</i> infection and greatly advance our understanding of adaptive
immunity in fungal infections.},
DOI = {10.32604/biocell.2024.051383}
}