Phagocytic killing and antibody response during the first year after tetravalent meningococcal vaccine in complement-deficient and in normal individuals

Citation
M. Schlesinger et al., Phagocytic killing and antibody response during the first year after tetravalent meningococcal vaccine in complement-deficient and in normal individuals, J CLIN IMM, 20(1), 2000, pp. 46-53
Citations number
20
Categorie Soggetti
Immunology
Journal title
JOURNAL OF CLINICAL IMMUNOLOGY
ISSN journal
02719142 → ACNP
Volume
20
Issue
1
Year of publication
2000
Pages
46 - 53
Database
ISI
SICI code
0271-9142(200001)20:1<46:PKAARD>2.0.ZU;2-I
Abstract
Seven individuals with late complement component (LCC) deficiency and seven control subjects were vaccinated with tetravalent meningococcal vaccine. T he response to vaccination was evaluated by measuring the antibody titer an d the phagocyte killing of the bacteria, before, 5-7 weeks, and 12-14 month s after vaccination. Prior to vaccination. no phagocytic killing and a low titer of antibody was found in the LCC-deficient group and a low killing (m ean of 40-58%, according to the serogroup) in normal controls. The phagocyt ic killing increased significantly 5-7 weeks after vaccination. However, wh ile in normal controls the phagocytic killing was close to 100% after 5-7 w eeks and decreased only slightly during the first year, the mean killing of the various meningococcal subgroups in LCC-deficient individuals was 70-89 % and dropped to only 53-71% one year after vaccination. Six weeks after va ccination the mean antimeningococcal antibody titer increased similarly in the sera of LCC-deficient patients and controls. One year after vaccination the controls maintained the high concentration, while the LCC-deficientpat ients had tendency toward a decrease. In addition, the interpersonal vari a bility of the antibody concentration, both in LCC-deficient individuals and in normal controls, was much higher than the phagocytic killing, with only a very mild increase in some individuals. Thus, it is possible that in spi te of adequate increase of antimeningococcal antibody titer after vaccinati on of LCC-deficient individuals their immunity against the bacteria may not be optimal. Our data show also that phagocytic killing of meningococci is probably a more consistent assay than antibody titer levels for antimeningo coccal immunity, especially in LCC-deficient patients.