Inherited maternal memory T cells protect offspring from respiratory viral infection through disease tolerance
Authors: H. Toure, B. Jimena, M. E. Caban, E. E. Lederer, D. M. Rico, A. Medlin McFadden, S. Abideen, P. Kokati, W. E. Harrington, M. A. Koch
Abstract
Maternal immune transfer is a powerful mechanism for early-life protection from infection, yet the full repertoire of protective factors remains unknown. We discovered that maternal memory T cells are both necessary and sufficient to protect offspring from lethal respiratory infection. This antigen-specific protection operated independently of maternal antibodies and offspring T cell responses and required IL-10 produced by maternal T cells. Transfer of protective maternal T cells reduced offspring inflammatory responses and lung tissue damage without affecting viral burdens, indicating that maternal memory T cells directly suppress pathogenic innate inflammatory responses to preserve offspring health. Critically, maternal vaccination similarly protected offspring in a T cell-dependent manner. These findings reveal maternal antigen-specific T cell transfer as a complementary immunological defense mechanism to protect offspring against pathogens that escape maternal antibodies, with broad implications for maternal vaccination strategies.
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Maternal mRNA Vaccination: Immunological Principles and Evidence Gaps in Infant ProtectionAikaterini I. Nikolaou, M. Matalliotakis, F. Ladomenou · 2026 · Vaccines · Not summarized yet
This narrative review examines maternal mRNA vaccination and antibody transfer for infant protection, while the paper tests maternal memory T-cell protection and vaccination.
Abstract
Maternal messenger RNA (mRNA) vaccination can generate maternal immunity and antibodies for passive infant protection. However, clinical evidence derives predominantly from the SARS-CoV-2 vaccines BNT162b2 and mRNA-1273, limiting generalization across the platform. This narrative review examines three questions: what determines maternal immune responses, what governs placental antibody transfer, and how immunological findings relate to infant clinical protection. Studies generally support preserved immune responsiveness during pregnancy, but associations with gestational timing are difficult to separate from dose number, previous infection, and time since antigen exposure. Transfer requires …
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TFAM Dependent Mitochondrial Fitness Limits CD8+ T Cell Immunopathology and Sustains Protective Immunity during Viral PneumoniaZ. Navaeiseddighi, Kai Guo, S. Hasan et al. · 2026 · bioRxiv · preprint, not peer reviewed · Not summarized yet
This study examines how CD8+ T-cell mitochondrial fitness affects antiviral immunity and lung immunopathology, whereas the paper studies transferred maternal T cells and offspring disease tolerance.
Abstract
During respiratory virus infections, CD8⁺ T cells kill virus-infected cells and establish antigen-specific immune memory, but excessive or dysregulated responses can also contribute to lung immunopathology. The development and maintenance of optimal CD8⁺ T cell effector and memory responses depend on mitochondrial fitness, which can be compromised across multiple physiologic and pathologic conditions. However, how impaired mitochondrial fitness affect antiviral CD8⁺ T cell responses remains poorly understood. Here, we used a CD8⁺ T cell-specific TFAM-haploinsufficient mouse model to induce moderate mitochondrial stress without the severe mitochondrial dysfunction associated with complete TFA…
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Trained immunity and related memory responses in lung health and diseaseXin-Yu Sun, Dan Zhao, Lei Zhang et al. · 2026 · Frontiers in Immunology · Not summarized yet
This review surveys innate immune memory in lung health and disease, whereas the paper identifies antigen-specific maternal T cells suppressing offspring lung inflammation.
Abstract
Immune memory has long been attributed to adaptive immunity, but trained immunity has broadened this view by showing that innate immune cells can retain altered function after prior stimulation and mount an enhanced response upon rechallenge. In the lung, prior local exposures can alter resident alveolar macrophages, whereas systemic immune stimulation can reprogramme bone-marrow progenitors and alter their myeloid output. Epithelial signals and alveolar-capillary barrier integrity help determine whether these changes protect tissue or promote injury. Reported metabolic pathways and chromatin features differ among cell types and experimental models; mTOR- and HIF-1α-mediated glycolysis and c…
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Trained Immunity in Childhood VaccinationChenrongrong Cai, L. Hossenbaccus, Eva Kaufmann · 2026 · Acta paediatrica · cited 1 time · Not summarized yet
This review discusses childhood vaccine protection through trained innate immunity, whereas the paper reports offspring protection from maternal vaccination through T cells.
Abstract
Conventionally, vaccine design has focused on identifying antigens that induce durable T and B cell memory and provide long term protection against subsequent encounters with the same pathogen. Unconventionally, a growing number of epidemiological, preclinical, and clinical studies demonstrate that live vaccines, including Bacillus Calmette Guérin (BCG), measles‐containing vaccines, and oral polio vaccine, induce protection through trained immunity, a form of metabolically and epigenetically mediated memory in innate immune cells and their progenitors. This concept is particularly relevant during early life, when adaptive immune responses are constrained and innate immunity represents the pr…
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Long-term immunoprophylaxis by TLR9 ligand mediates macrophage-ILC cross-talk against respiratory viral infectionAsuka Joy Tobuse, K. Kobiyama, Jun Tsuchida et al. · 2026 · Science Advances · Not summarized yet
This study uses intranasal TLR9 stimulation to induce antigen-independent innate protection against respiratory viruses, unlike the paper’s antigen-specific maternal T-cell transfer.
Abstract
Rapid development of host immunity is critical during the emergence of viral outbreaks when vaccines are not yet available. Here, we demonstrate that CpG oligodeoxynucleotide-schizophyllan complex (K3-SPG) induces antigen-independent, long-term protection against lethal respiratory virus infection. A single intranasal administration successfully enhanced host resistance to infection for as long as 100 days posttreatment. Mechanistically, we observed a lung-restricted biphasic innate activation of macrophages and innate lymphoid cells. Early protection was mediated by CD11b+CD11c+ macrophages (DP MΦ) and monocyte-derived interstitial macrophages (IMΦ). Late protection was mediated by innate l…
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The transition to postpartum lactation establishes a state of maternal antiviral resilienceAriana Campbell, Taylor Miller-Ensminger, M. C. Arreguin et al. · 2026 · bioRxiv · preprint, not peer reviewed · Not summarized yet
This paper concerns maternal antiviral resilience after childbirth, while the paper examines maternal memory T-cell transfer protecting offspring from respiratory infection.
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Temporal and transcriptional programming of effector memory B cells shapes vaccine platform-dependent humoral immunityAnoma Nellore, Christopher Fucile, Christopher D. Scharer et al. · 2026 · iScience · Not summarized yet
This study compares vaccine-platform effects on influenza-specific memory B cells and antibody outcomes, whereas the paper focuses on maternal T-cell-mediated protection of offspring.
Abstract
Summary This study investigates how influenza vaccine platform shapes the memory B cell responses that underlie durable antibody protection. Using fluorescent hemagglutinin (HA) probes, the authors compared HA-specific IgD-negative B cells in adults who received either live attenuated influenza vaccine (LAIV) or inactivated influenza vaccine (IIV). Both platforms induced circulating T-bet+ HA+ B cells with similar phenotypic features, but their relationship to antibody outcomes diverged sharply: while these cells track with durable IgG responses after IIV, only early (day 7–14) T-bet+ HA+ B cell frequencies predicted durable IgA responses after LAIV. Single-cell transcriptional profiling fur…
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Immune system ontogeny—a subtle evolution to perfectionA. Munteanu, M. Surcel, Elena-Georgiana Dobre et al. · 2026 · Frontiers in Aging · Not summarized yet
This review discusses newborn immune development and vulnerability to infection, providing developmental context for the paper’s study of transferred maternal protection.
Abstract
It is well known that both innate and adaptive immune systems in newborns are immature, making them highly susceptible to infection. Additionally, pre-term newborns with hindered immune systems are more prone to increased mortality and morbidity. Newborns are capable of mounting adaptive immune responses, but their capability to develop long-lasting immunity is limited. Thus, the fetus and newborn’s immune system is considered “immature” due to functional disorders in immune response or suppression by regulatory cells. Aging is another factor that leads to impaired immune responses due to a state of chronic low-grade inflammation (inflammaging), which compromises defense against pathogens an…
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Updated on 9 November 2026.