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Updated: Sep 23, 2026

Evaluation of Host-Pathogen Responses and Vaccine Efficacy in Mice
Published on: February 22, 2019
Measles and mumps vaccination as a model to investigate the developing immune system: passive and active immunity
Hayley Gans1, Ross DeHovitz, Bagher Forghani
1Department of Pediatrics, Stanford University School of Medicine, 300 Pasteur Drive, Rm G312, Stanford, CA 94305-5208, USA.
Insights
Infants under 12 months show reduced antibody responses to vaccines due to passive immunity and intrinsic deficiencies. However, T-cell responses are induced, suggesting maternal vaccination can enhance infant immunity.
Area of Science:
- Immunology
- Vaccinology
- Pediatrics
Background:
- Infant immune responses to vaccines are complex, influenced by maternal antibodies and developmental stage.
- Understanding primary vaccine failure in infants is crucial for optimizing immunization schedules.
Purpose of the Study:
- To evaluate neutralizing antibody and T-cell responses in infants vaccinated at different ages (6, 9, 12 months).
- To clarify the role of passive antibody effects and intrinsic infant immunity on vaccine response.
- To assess the impact of a second measles vaccine dose and maternal immunization strategies.
Main Methods:
- Infants aged 6, 9, and 12 months received measles or mumps vaccines.
- Neutralizing antibody titers, T-cell proliferation, and interferon-gamma (IFNγ) production were measured.
- Infants received a second measles vaccine dose at 12-15 months if previously vaccinated.
Main Results:
- Six-month-olds exhibited diminished humoral immunity due to passive antibodies and intrinsic deficiencies.
- Nine-month-olds' lower titers were solely linked to passive antibody effects.
- Vaccination at all ages induced measles- and mumps-specific T-cell responses, irrespective of passive antibodies.
- A second measles dose improved T-cell responses and seroconversion rates in younger infants.
Conclusions:
- Passive antibodies can interfere with infant humoral immunity but not T-cell sensitization.
- Maternal immunization strategies may enhance passive antibody protection and infant adaptive immunity.
- Infant T-cell responses under maternal antibody "cover" prime for future exposures, supporting synergistic protection.
Abstract:
Evaluations of neutralizing antibody responses in 6-, 9- and 12-month-old infants given measles or mumps vaccine indicated that 6-month-old infants had diminished humoral immune responses associated with passive antibody effects, but also had an intrinsic deficiency in antiviral antibody production, which was independent of passive antibody effects. In contrast, lower neutralizing antibody titers in 9-month-olds were related only to passive antibody effects. Measles and mumps-specific T-cell proliferation and interferon-gamma (IFNgamma) production were induced by vaccination at 6, 9 or 12 months, regardless of passive neutralizing antibodies or age. These observations suggest a need to refine concepts about passive antibody interference and primary vaccine failure, taking into account the sensitization of antiviral T-cells, which occurs in the presence of passive antibodies and is observed in infants who do not develop active humoral immunity. A second dose of measles vaccine given at 12-15 months enhanced antiviral T-cell responses to measles in infants who were vaccinated at 6 or 9 months, and produced higher seroconversion rates. Since T-cell immunity is elicited under the cover of passive antibodies, the youngest infants benefit from the synergistic protection mediated by maternal antibodies and their own capacity to develop sensitized antiviral T-cells, which prime for subsequent exposures to the viral antigens. Conceptually, maternal immunization approaches with vaccines that can be given to women of child-bearing age before pregnancy, or that are safe for administration during pregnancy, should enhance passive antibody protection. Rather than being detrimental to infant adaptive immune responses, maternal vaccination can be coupled effectively with vaccine regimens that elicit priming of antiviral immune responses in infants during the first year of life.
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