“…Agspecific memory B cells have been detected in peripheral blood many years following immunization of adults with protein vaccines. In one study there was a frequency of 0.01-1% of total IgGsecreting memory B cells for diphtheria and 0.1-1% for tetanus (27). Another study detected smallpox-specific memory B cells .50 y following immunization at a frequency of 0.1% of total IgG-secreting memory cells (23).…”
Section: Discussionmentioning
confidence: 99%
“…Memory B cells have been consistently shown to increase in frequency in the circulation following immunization (23,27,29,39), when newly generated Ag-specific memory B cells may be transiting through the circulation to other lymphoid tissues. Following a booster, Ag-specific memory B cells are detected at the end of the first week and are persistent for at least 1 mo (28,29,39).…”
Section: Menc-specific Memory B Cell Immune Responses Postboostermentioning
confidence: 99%
“…These studies suggest that even in the absence of re-exposure to an Ag, memory B cells continuously divide and differentiate into plasma cells either spontaneously or via intermittent Ag-independent mechanisms such as microbial products (polyclonal stimulation of B cells via TLRs), cytokines (secreted by T cells activated by another Ag, also known as bystander T cell help), or possibly other as yet unknown stimuli (24). Consequently, this theory suggests that memory B cells continuously recirculate through the blood and secondary lymphoid organs (27), and therefore circulating levels of Ab are in proportion to the total Ag-specific memory B cell pool that is reflected by the frequency of circulating Ag-specific B cells. This theory is supported by a B cell kinetic study in humans (47).…”
Section: Menc-specific Memory B Cell Immune Responses Postboostermentioning
The maintenance of adequate serum Ab levels following immunization has been identified as the most important mechanism for individual long-term protection against rapidly invading encapsulated bacteria. The mechanisms for maintaining adequate serum Ab levels and the relationship between Ag-specific memory B cells and Ab at steady state are poorly understood. We measured the frequency of circulating serogroup C meningococcal (MenC)-specific memory B cells in 250 healthy 6- to 12-y-old children 6 y following MenC conjugate vaccine priming, before a booster of a combined Haemophilus influenzae type b–MenC conjugate vaccine and then 1 wk, 1 mo, and 1 y after the booster. We investigated the relationship between circulating MenC-specific memory B cell frequencies and Ab at baseline and following the booster vaccine. We found very low frequencies of circulating MenC-specific memory B cells at steady state in primary school-aged children and little association with MenC IgG Ab levels. Following vaccination, there were robust memory B cell booster responses that, unlike Ab levels, were not dependent on age at priming with MenC. Measurement of B cell memory in peripheral blood does not predict steady state Ab levels nor the capacity to respond to a booster dose of MenC Ag.
“…Agspecific memory B cells have been detected in peripheral blood many years following immunization of adults with protein vaccines. In one study there was a frequency of 0.01-1% of total IgGsecreting memory B cells for diphtheria and 0.1-1% for tetanus (27). Another study detected smallpox-specific memory B cells .50 y following immunization at a frequency of 0.1% of total IgG-secreting memory cells (23).…”
Section: Discussionmentioning
confidence: 99%
“…Memory B cells have been consistently shown to increase in frequency in the circulation following immunization (23,27,29,39), when newly generated Ag-specific memory B cells may be transiting through the circulation to other lymphoid tissues. Following a booster, Ag-specific memory B cells are detected at the end of the first week and are persistent for at least 1 mo (28,29,39).…”
Section: Menc-specific Memory B Cell Immune Responses Postboostermentioning
confidence: 99%
“…These studies suggest that even in the absence of re-exposure to an Ag, memory B cells continuously divide and differentiate into plasma cells either spontaneously or via intermittent Ag-independent mechanisms such as microbial products (polyclonal stimulation of B cells via TLRs), cytokines (secreted by T cells activated by another Ag, also known as bystander T cell help), or possibly other as yet unknown stimuli (24). Consequently, this theory suggests that memory B cells continuously recirculate through the blood and secondary lymphoid organs (27), and therefore circulating levels of Ab are in proportion to the total Ag-specific memory B cell pool that is reflected by the frequency of circulating Ag-specific B cells. This theory is supported by a B cell kinetic study in humans (47).…”
Section: Menc-specific Memory B Cell Immune Responses Postboostermentioning
The maintenance of adequate serum Ab levels following immunization has been identified as the most important mechanism for individual long-term protection against rapidly invading encapsulated bacteria. The mechanisms for maintaining adequate serum Ab levels and the relationship between Ag-specific memory B cells and Ab at steady state are poorly understood. We measured the frequency of circulating serogroup C meningococcal (MenC)-specific memory B cells in 250 healthy 6- to 12-y-old children 6 y following MenC conjugate vaccine priming, before a booster of a combined Haemophilus influenzae type b–MenC conjugate vaccine and then 1 wk, 1 mo, and 1 y after the booster. We investigated the relationship between circulating MenC-specific memory B cell frequencies and Ab at baseline and following the booster vaccine. We found very low frequencies of circulating MenC-specific memory B cells at steady state in primary school-aged children and little association with MenC IgG Ab levels. Following vaccination, there were robust memory B cell booster responses that, unlike Ab levels, were not dependent on age at priming with MenC. Measurement of B cell memory in peripheral blood does not predict steady state Ab levels nor the capacity to respond to a booster dose of MenC Ag.
“…Memory B cells make a significant contribution to protective immunity and are characterized in terms of (1) a rapid proliferative response, accompanied by cellular differentiation after antigen reexposure, to produce affinity-matured, antibody-secreting plasma cells; (2) a lower activation threshold, compared with that of naive B cells, in response to cytokine and antigen; and (3) an absence of spontaneous immunoglobulin secretion. Recently, the identification of antigen-specific memory B cells against vaccine antigens (diphtheria and tetanus), whereby isolated peripheral-blood mononuclear cells (PBMCs) were nonspecifically stimulated by bacterial antigens and interleukin-2 (IL-2), followed by the specific detection of antigen-specific memory B cells, has been described [13]. This approach may also prove to be useful in the elucidation of virus-specific B cell-mediated immunity.…”
Background. Loss of antibody reactivity against linear epitopes of parvovirus B19 (B19) capsid proteins VP1 and VP2 occurs after infection; however, it is unclear whether B cell memory is established against linear epitopes.Methods. B cell enzyme-linked immunospot assay was used to evaluate B19-specific B cell memory in volunteer donors ( ). n p 22 Results. B cell memory is maintained against conformational epitopes of VP2 and is absent against linear epitopes of VP2. Individuals seronegative for IgG against the unique region of VP1 have detectable B cell memory, with the potential to mount a humoral response on reexposure to B19. Conversely, in mice immunized with VP2, long-lasting IgG against linear epitopes of VP2 and a strong B cell-memory response are observed.Conclusions. B cell memory is established and maintained against conformational epitopes of VP2 and against linear epitopes of VP1 but not against linear epitopes of VP2. These findings further our understanding of the immune response to B19 and suggest that analysis of B19-specific B cell memory merits consideration for future B19-vaccine studies.
“…It is therefore essential that any in vitro assay of TT vaccine immunogenicity measure the capacity of the vaccine to induce specific antibodies. Due to the sensitivity of the ELISPOT assay for quantifying the number of producing cells, this was applied to the measurement of anti-TT antibody production [15]. High levels of TT-specific antibody-secreting B-cells were visualised following the in vitro stimulation of PBMCs with TT antigen (Fig.…”
Section: Immune Activation In Vitro Measured By Antibody Elispotmentioning
Many vaccines employed in childhood vaccination programmes are produced by conventional techniques, resulting in complex biological mixtures for which batch-related quality control requires in vivo potency testing. Monitoring consistency via in vitro tests during the vaccine production has the capacity to replace certain of the in vivo methods. In this respect, determining vaccine antigen immunogenicity through functional immunological tests has high potential. Advances in immunology have made it possible to analyse this biological activity by in vitro means. The present study established such an in vitro test system for tetanus toxoid (TT). This measured vaccine immunogenicity through an antigen-specific secondary (recall) response in vitro, using a porcine model growing in value for its closeness to human immune response characteristics. Discrimination between the specific recall TT antigen and diphtheria toxoid (DT) was possible using both peripheral blood mononuclear cell cultures and monocyte-derived dendritic cells in co-culture with autologous specific lymphocytes. TT-specific activation was detected with highest discrimination capacity using proliferation assays, as well as IFN-gamma and TT-specific antibody ELISPOTS (measuring secreting T and B lymphocytes, respectively). These in vitro systems show a high potential for replacing animal experimentation to evaluate the immunogenicity of complex vaccines.
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