Long-term presence of memory B-cells specific for different vaccine components.

Vaccination against infectious diseases ideally should provide lifelong immunity, but in many cases waning of antibody titers has been observed over time. In this study we describe the identification of antigen-specific memory B-cells in peripheral blood of persons born between 1940 and 2004 in The Netherlands. Polyclonal stimulation of either PBMCs or purified B-cells induced proliferation and differentiation of B-cells of the memory phenotype (CD19(+)/CD27(+)) into antibody secreting cells (ASC). Memory B-cells against components of bacterial vaccines (Bordetella pertussis and tetanus) as well as viral vaccines (measles and influenza) were thus identified, even in persons with low serum antibody titers. Enrichment of B-cells increased the sensitivity of memory B-cell detection when compared to PBMCs. Low, but significant correlations between numbers of antigen-specific memory B-cells and the corresponding circulating antibody titers were found for the pertussis proteins and measles virus, but not for tetanus. The identification of the numbers and specificities of peripheral memory B-cells and their relationship with circulating antibodies may be very useful to determine the long-term efficacy of vaccination.

Timing of infection and prior immunization with respiratory syncytial virus (RSV) in RSV-enhanced allergic inflammation.

Respiratory syncytial virus (RSV) infection has been shown to be a risk factor for the development of allergy in humans and mice. The allergy-enhancing properties of RSV may be dependent on atopic background and an individual's history of RSV infection. We examined the influence of the timing of infection and prior inoculation with RSV in a mouse model of allergic asthma. Mice were sensitized to and challenged with ovalbumin (OVA) and were inoculated with RSV either before or during the sensitization or challenge period. One group of mice was inoculated with RSV both before sensitization to OVA and during challenge with OVA. Increased pulmonary expression of interleukin (IL)-4, IL-5, and IL-13 mRNA and aggravated alveolitis and hypertrophy of mucus-producing cells were observed only when OVA-sensitized mice were inoculated with RSV shortly before or during challenge with OVA. Despite protection against viral replication, prior inoculation with RSV did not abrogate RSV-enhanced, OVA-induced expression of T helper 2 (Th2) cytokines in the lung. In conclusion, inoculation with RSV enhances allergic disease only when the immune system has already been Th2-primed by the allergen (i.e., OVA). This RSV-enhanced allergy is not completely abrogated by prior inoculation with RSV.