Measles and mumps vaccination as a model to investigate the developing immune system: passive and active immunity during the first year of life.
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.
Gans
Hayley
H
Department of Pediatrics, Stanford University School of Medicine, 300 Pasteur Drive, Rm G312, Stanford, CA 94305-5208, USA.
DeHovitz
Ross
R
Forghani
Bagher
B
Beeler
Judith
J
Maldonado
Yvonne
Y
Arvin
Ann M
AM
D000375:Aging / Q000276:immunology; D000917:Antibody Formation / Q000276:immunology; D015704:CD4 Antigens / Q000276:immunology; D006801:Humans; D007107:Immune System / Q000254:growth & development* / Q000276:immunology*; D007110:Immunity, Active / Q000276:immunology*; D007116:Immunization, Passive; D007223:Infant; D007231:Infant, Newborn; D007371:Interferon-gamma / Q000096:biosynthesis / Q000276:immunology; D018664:Interleukin-12 / Q000096:biosynthesis / Q000276:immunology; D008458:Measles Vaccine / Q000276:immunology*; D009108:Mumps Vaccine / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology; D014611:Vaccination
D015704:CD4 Antigens; D008458:Measles Vaccine; D009108:Mumps Vaccine; D018664:Interleukin-12; D007371:Interferon-gamma