Key result
Absent cytokines yield non-cytotoxic neonatal CD8 T cells, increasing early-life MCMV lung disease risk.
Why the study?
Differential antiviral T cell immunity in early life impacts CMV clinical outcomes, but the underlying mechanisms are not well understood.
Does adoptive transfer of adult T cells or cytokine supplementation improve control of lung MCMV infection in neonatal mice?
Population
Model of respiratory murine CMV infection in early life and neonates
Comparison
Adoptive T cell transfers and cytokine supplementation vs controls
Design
Preclinical animal model and adoptive transfer study
Authors
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Early-life T cell immunity may heighten infant CMV morbidity; leaves open age-adapted mechanistic therapies pending human validation.
Does adoptive transfer of adult T cells or cytokine supplementation improve control of lung MCMV infection in neonatal mice?
Defective CD8 T cell priming due to absent key cytokines in neonates explains the higher risk for MCMV lung disease in early life.
Brito et al. (2026) studied Murine cytomegalovirus (MCMV) infection. Adoptive T cell transfer and cytokine supplementation was evaluated on MCMV-specific T cell responses and infection control. Defective CD8 T cell priming in neonates, driven by absent key cytokines, leads to non-cytotoxic CD8 effector T cells and explains the higher risk for early-life MCMV lung disease.
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