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Immunodeficiency and Autoimmune Disorders · Journal article
The Journal of Immunology · July 28, 2026
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In mice, β-glucan administered intraperitoneally seven days before intranasal RSV infection reduced total CD8 tissue resident memory (Trm) cell numbers and function in airways 30 days post-infection compared to RSV infection alone, without affecting acute disease severity. This preclinical finding suggests that trained immunity induction via β-glucan may have unintended immunological consequences for T cell memory responses to respiratory viral infection.
Controlled preclinical intervention study in mice. Laboratory mice; specific strain, age, and sex not stated in abstract.. Intervention: Intraperitoneal injection of β-glucan seven days prior to intranasal RSV infection. Compared with: RSV infection alone (vehicle control).
β-glucan pretreatment resulted in significant decrease in total CD8 Trm number in airways at 30 days post-RSV infection β-glucan pretreatment resulted in significant decrease in CD8 Trm function in airways at 30 days post-RSV infection RSV disease severity (measured by weight loss and airway obstruction) was not impacted by prior β-glucan treatment
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These preliminary findings raise concern about the use of β-glucan as a vaccine adjuvant for respiratory viral infections, suggesting it may paradoxically impair protective T cell memory formation. However, translation to humans requires validation and assessment of whether the observation generalizes to other trained immunity stimuli or infection contexts.
Mechanistic mouse study showing β-glucan-induced trained immunity impairs lung CD8 Trm formation after RSV infection, but lacks clinical translation and comparator arm specificity.
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These preliminary findings raise concern about the use of β-glucan as a vaccine adjuvant for respiratory viral infections, suggesting it may paradoxically impair protective T cell memory formation. However, translation to humans requires validation and assessment of whether the observation generalizes to other trained immunity stimuli or infection contexts.
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Abstract Introduction Trained immunity is a well-documented phenomenon which can mediate non-specific immunity against pathogens. Secondary challenge following training results in increased production of proinflammatory mediators by innate immune cells. It has been previously shown that this inflammatory microenvironment can influence T cell responses and may alter the Th1/Th2 and Treg/Th17 balance. Here we examined the impact of trained immunity on lung tissue resident memory (Trm) formation and function following respiratory syncytial virus (RSV) infection. Methods Mice were treated intraperitoneally (i.p.) with compounds known to induce trained immunity seven days prior to intranasal infection with RSV. Disease severity was measured via weight loss and airway obstruction throughout initial training and subsequent RSV infection. Lungs and bronchoalveolar lavage (BAL) fluid were harvested 30 days post-RSV infection. Cells from the lung and BAL were stimulated ex vivo with RSV peptides to determine Trm cytokine production. Cells were then characterized using spectral flow cytometric analysis. Results Mice administered β-glucan i.p. prior to RSV infection exhibited a significant decrease in total CD8 Trm number and function in the airways at 30 days post-infection compared to RSV infection alone. RSV disease severity was not impacted by prior β-glucan treatment. Conclusion β-glucan is a well characterized trained immunity stimulus and is a promising adjuvant in vaccine development, with several ongoing clinical trials for both cancer and viral studies. However, our results suggest that β-glucan induced training decreases Trm numbers and function following RSV infection, highlighting the need for further studies in this area. Funding Source N/A Topic Categories Viral Immunology (VIR)
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