Considerable evidence indicates that complement-mediated serum bactericidal antibody (SBA), induced by nasopharyngeal colonization or vaccination, confers protection against MenB [3] and [4]. Soluble antibodies maintain a first line of defence to extracellular pathogens both systemically and at mucosal surface and are recognised as Selleck GSK-3 inhibitor serological memory. In contrast, memory-B cells are able to provide more antibody-producing cells (ASC) after re-exposure to specific antigens or polyclonal stimuli [5] and [6]. Ideally, vaccination against N. meningitidis should provide protection for life by the continuous production of high titers of specific antibodies or the ability to respond rapidly to mount

for an anamnestic antibody response [7]. Besides the Libraries memory antibody response, the cellular pattern of immune response has an important role in maintenance of immunological memory. Three subsets of T-cells have been identified based on expression patterns of CD45RA and the chemokine receptor

CCR7 [8]. Two subsets represent in fact different stages of maturation with CD45RA−CCR7+ central memory T-cells (TCM) being the least differentiated, CD45RA−CCR7− effector memory T-cells (TEM) representing an intermediate stage, and CD45RA+CCR7− effector terminally differentiated T-cells (TET) being the most differentiated Galunisertib price ones [9]. Determination of the expression of surface antigens is an alternative method for evaluating the lymphocyte effector function [10]. The CD69 antigen has been identified as the earliest activation marker on the surfaces of antigen- or allergen-specific activated lymphocytes in vitro [11]. Once CD69 is expressed, it acts as a co-stimulatory molecule for T-cell activation and proliferation [12].

Understanding the mechanism by which meningococcal vaccines generate and sustain the serological and cellular immune memory is essential science to improving the long-term efficacy of MenB vaccines. We have previously shown that MenB vaccine induced a strong ASC primary response in mice, but the recall response showed a limited power over time. Nonetheless, memory B-cells were maintained over the time and were probably responsible for the strong antibody response seen after booster vaccination [13]. In the present study, we investigated the development of long-term humoral and cellular (ASC, memory B-cells, memory/effector T-cells) responses after immunisation of health subjects with the VA-MENGOC-BC® vaccine. Functional antibody analyses were investigated by bactericidal and opsonic assays using the homologous strain and strains lacking PorA or Opa proteins as the target strains. Six healthy volunteers (5 women and 1 man) aged 23–45 were enrolled in this study. Vaccination and venipuncture was done with the consent of the donors after the nature and possible consequences of the study had been fully explained.