ArticleThe Journal of infectious diseases2026
MHC-I Upregulation and Increased Glucose Dependence Define Innate Antifungal Immune Responses to Cryptococcus neoformans.
Article in The Journal of infectious diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
backgroundCryptococcus neoformans, the etiologic agent of cryptococcosis, can survive and replicate within host immune cells, contributing to development of cryptococcal meningitis. Within the lung, C neoformans interacts with innate immune subsets, including macrophages and dendritic cells (DCs). Our previous work demonstrated that Ly6c- monocyte-like macrophages restrict fungal proliferation, whereas CD11b+ DCs promote fungal growth. Transcriptomic profiling revealed differential expression of MHC-I gene H2-K1, calreticulin, and metabolic genes. Therefore, we hypothesized that H2-K1 and metabolic pathways modulate intracellular fungal fate within pulmonary macrophages and DCs.
methodsH2-K1 expression was knocked down by siRNA in J774 macrophages and bone marrow-derived DCs induced by granulocyte-macrophage colony-stimulating factor. Antifungal activity was determined by colony-forming unit enumeration. Phagocytic uptake, cathepsin B activity, Nos2 expression, and reactive oxygen species production were quantified by flow cytometry. Metabolic dependencies were evaluated through SCENITH assay (single-cell energetic metabolism by profiling translational inhibition).
resultsH2-K1 knockdown in J774 cells significantly reduced antifungal activity as compared with controls. H2-K1 knockdown also decreased calreticulin gene expression, suggesting that H2-k1 has downstream effects in the pathway. H2-K1 silencing did not significantly alter phagocytic uptake, cathepsin B activity, or Nos2 expression. However, reactive oxygen species production was significantly reduced in H2-K1 knockdown J774 cells, indicating impaired responses. SCENITH analysis revealed that antifungal macrophages shift their metabolism toward glucose oxidation for ATP generation, which is important for antifungal activity.
conclusionsThese findings indicate that metabolic reprogramming is critical for effective antifungal responses. Our data provide a foundation for future studies aimed at targeting host immune and metabolic pathways to enhance antifungal immunity.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.