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Credit: Pixabay\/CC0 Public Domain<\/p>\n
At the surface, the immune response to a flu virus is simple. Some cells recognize the pathogen and send a signal to the immune system, and immune cells produce a potentially lifesaving antibody against the virus. Antigen in, antibody out.<\/p>\n
However, details of the intervening steps, as researchers have learned in the past 65 years, are quite complex\u2014certain cells carry the flu antigen to the immune system<\/a>, specific immune cells<\/a> respond to the antigen and touch and interact with each other to evoke a response, antibody genes<\/a> in each responsive B cell undergo many somatic mutations to create a panoply of potential specific antibodies, antibody classes like IgM and IgG are switched, cells producing the least fit antibodies are eliminated, and the survivors that produce the best flu-specific antibody boost their metabolism to produce massive amounts of the antibody protein.<\/p>\n Less well understood, but also complex, is the memory immune response<\/a> to influenza, the creation of sentinel immune cells that stand on guard against subsequent infections. These long-lived memory cells have reacted to the flu antigen but avoid the irreversible pathway of antibody production. Instead, they wait quiescently in lungs and lymph nodes<\/a>, primed to quickly transform into antibody-producing cells if a flu virus<\/a> attacks again.<\/p>\n In a study<\/a> published in the journal Immunity, Fran Lund, Ph.D., professor of microbiology and director of the University of Alabama at Birmingham Immunology Institute, and colleagues describe six subsets of memory B cells\u2014including one subset that produces the transcription factor T-bet. Using detailed genetic analysis and manipulation, they show that continuous T-bet expression in these cells is key to preserving the protective memory response. In a mouse influenza model, they found that T-bet expression was required for the persistence of lung and lymph node memory B cells that have rapid differentiation potential to become antibody-producing plasma cells.<\/a><\/p>\n T-bet is a transcription factor, one of the control proteins in the cell nucleus<\/a> that can turn specific groups of genes on and off. Cohorts of different transcription factors orchestrate diverse sets of genes that alter cell function and differentiation.<\/p>\n Previous studies had shown some association of T-bet expression with attributes of human, vaccine-specific memory B cells and with a long-lived humoral response to infection by mouse, virus-specific germinal center B cells.<\/p>\n To better understand T-bet-expressing memory B cells, UAB researchers infected mice with flu virus. Thirty days after infection, they isolated mature memory B cells that were specific for response to the influenza NP antigen and used single-cell sequencing to identify the gene expression of each cell. Gene-expression data of these individual cells comprised seven distinct clusters.<\/p>\n One cluster was excluded as developmentally distinct, and the other six were analyzed in detail, including core transcriptional regulators, the B-cell receptor repertoires and the functional attributes of each the gene expression in each cluster. T-bet was highly expressed and upregulated in cluster 2. Cluster 2 was also enriched for expression of genes reported to be upregulated in flu vaccine-elicited, T-bet-expressing human effector memory B cells. Enriched genes for protein synthesis in cluster 2 cells suggested a shift from the memory B cell identity program toward the antibody-producing program. While only the cluster 2 gene expression showed effector memory B cell characteristics, other clusters showed distinct stem-like, tissue surveilling or inflammatory characteristics.<\/p>\n Researchers used constitutive or inducible deletions of the T-bet gene from B cells to show that T-bet identifies flu infection-elicited lymph node and lung memory B cells that have rapid differentiation potential to antibody-secreting cells, and that T-bet expression by lung memory B cells was needed for a secondary lung antibody-secretion response following a second exposure to flu virus. In the future, the authors hope to use these data to design new ways to induce T-bet expression in human memory B cells to elicit memory cells that will reside at local sites of infection and can provide early protection from infection.<\/p>\n More information:<\/strong> \t\t\t\t\t\t\t\t\t\t\t\tProvided by \t\t\t\t\t\t\t\t\t\t\t\t\t<\/a><\/p>\n \n Citation<\/strong>: \n This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no
\n Christopher A. Risley et al, Transcription factor T-bet regulates the maintenance and differentiation potential of lymph node and lung effector memory B cell subsets, Immunity (2025). DOI: 10.1016\/j.immuni.2025.05.021<\/a><\/p>\n
\n\t\t\t\t\t\t\t\t\t\t\t\t\t\t\t\t\t\t\t\t\t\t\t\t\tUniversity of Alabama at Birmingham<\/a>
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\n T-bet protein found essential for maintaining flu-fighting memory B cells (2025, July 12)
\n retrieved 12 July 2025
\n from https:\/\/medicalxpress.com\/news\/2025-07-protein-essential-flu-memory-cells.html\n <\/p>\n
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