Background: Acute myeloid leukemia (AML) is a prevalent and potentially fatal hematologic malignancy with limited improvements in survival rates over the past few decades. ITGAM, encoding CD11b, is a significant integrin component in leukocytes, involved in various biological processes. However, its role in AML prognosis and immune cell infiltration remains poorly understood.
Methods: This study investigated the prognostic significance and potential function of ITGAM in AML using comprehensive bioinformatic analyses.
Results: ITGAM expression was markedly upregulated in AML patients, correlating with advanced age (> 60 years), French-American-British (FAB) classification subtypes M4 and M5, and intermediate or poor cytogenetic risk. Gene enrichment analysis revealed that ITGAM was involved in immune system regulation and was positively associated with the infiltration of neutrophils, immature dendritic cells, and macrophages in AML. Notably, the expression of ITGAM was linked to increased infiltration of immunosuppressive subsets of these innate immune cells, which may partially explain its association with a poorer prognosis.
Conclusion: These findings suggest that ITGAM could serve as a valuable prognostic biomarker in AML, reflecting an adverse prognosis associated with enhanced infiltration of immunosuppressive innate immune cells.
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http://dx.doi.org/10.1111/ijlh.14444 | DOI Listing |
J Immunol
January 2025
Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, United States.
Current influenza vaccines are not effective in conferring protection against antigenic variants and pandemics. To improve cross-protection of influenza vaccination, we developed a 5xM2e messenger RNA (mRNA) vaccine encoding the tandem repeat conserved ectodomain (M2e) of ion channel protein M2 derived from human, swine, and avian influenza A viruses. The lipid nanoparticle (LNP)-encapsulated 5xM2e mRNA vaccine was immunogenic, eliciting high levels of M2e-specific IgG antibodies, IFN-γ+ T cells, T follicular helper cells, germinal center phenotypic B cells, and plasma cells.
View Article and Find Full Text PDFJ Immunol
January 2025
Key Laboratory of Breeding Biotechnology and Sustainable Aquaculture, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, P. R. China.
The von Hippel-Lindau (VHL) tumor suppressor gene VHL is a classic tumor suppressor that has been identified in family members with clear cell renal cell carcinomas, central nervous system and retinal hemangioblastomas, phaeochromocytomas, and pancreatic neuroendocrine tumors. The well-defined function of VHL is to mediate proteasomal degradation of hydroxylated hypoxia-inducible factor α proteins, resulting in the downregulation of hypoxia-responsive gene expression. Previously, we reported that VHL inhibits antiviral signaling by targeting mitochondrial antiviral signaling protein (MAVS) for proteasomal degradation.
View Article and Find Full Text PDFJ Immunol
January 2025
Biotechnology Department, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, Consejo Superior de Investigaciones Científicas, Madrid, Spain.
Upon antigen encounter, B cells start a differentiation process toward antibody-secreting cells (ASCs), initially plasmablasts, and eventually long-lived plasma cells. All these ASCs specialize in secreting important amounts of antibodies and usually lose other functionalities of naïve B cells. This differentiation process is scarcely characterized in teleost fish, in which B cells have been shown to share many functional and phenotypic characteristics of mammalian B1 innate subsets.
View Article and Find Full Text PDFJ Immunol
February 2025
Department of Pharmacology and Toxicology, University of Arizona, Tucson, AZ, United States.
Mitochondrial antiviral-signaling protein (MAVS) is a key adapter protein required for inducing type I interferons (IFN-Is) and other antiviral effector molecules. The formation of MAVS aggregates on mitochondria is essential for its activation; however, the regulatory mitochondrial factor that mediates the aggregation process is unknown. Our recent work has identified the protein Aggregatin as a critical seeding factor for β-amyloid peptide aggregation.
View Article and Find Full Text PDFJ Immunol
February 2025
La Jolla Institute for Immunology, La Jolla, CA, United States.
A fundamental dichotomy in lymphocytes separates adaptive T and B lymphocytes, with clonally expressed antigen receptors, from innate lymphocytes, which carry out more rapid responses. Some T cell populations, however, are intermediates between these 2 poles, with the capacity to respond rapidly through T cell receptor activation or by cytokine stimulation. Here, using publicly available datasets, we constructed linear mixed models that not only define a gradient of innate gene expression in common for mouse innate-like T cells, but also are applicable to other mouse T lymphoid populations.
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