scholarly journals High Titers of Circulating Maternal Antibodies Suppress Effector and Memory B-Cell Responses Induced by an Attenuated Rotavirus Priming and Rotavirus-Like Particle-Immunostimulating Complex Boosting Vaccine Regimen

2006 ◽  
Vol 13 (4) ◽  
pp. 475-485 ◽  
Author(s):  
Trang V. Nguyen ◽  
Lijuan Yuan ◽  
Marli S. P. Azevedo ◽  
Kwang-il Jeong ◽  
Ana M. Gonzalez ◽  
...  
Keyword(s):  
B Cell ◽  
Immunoglobulin A ◽  
Lymphoid Tissues ◽  
Memory B Cell ◽  
Antibody Secreting Cell ◽  
Cell Responses ◽  
Rotavirus Vaccines ◽  
Virus Like Particle ◽  
Antibody Titers ◽  
B Cell Responses

ABSTRACT We investigated maternal antibody (MatAb) effects on protection and immune responses to rotavirus vaccines. Gnotobiotic pigs were injected intraperitoneally at birth with pooled serum from sows hyperimmunized with human rotavirus (HRV); control pigs received no sow serum. Pigs with or without MatAbs received either sequential attenuated HRV (AttHRV) oral priming and intranasal boosting with VP2/VP6 virus-like particle (VLP)-immunostimulating complex (ISCOM) (AttHRV/VLP) or intranasal VLP-ISCOM prime/boost (VLP) vaccines at 3 to 5 days of age. Subsets of pigs were challenged at 28 or 42 days postinoculation with virulent Wa HRV to assess protection. Isotype-specific antibody-secreting cell (ASC) responses to HRV were quantitated by enzyme-linked immunospot assay to measure effector and memory B-cell responses in intestinal and systemic lymphoid tissues pre- and/or postchallenge. Protection rates against HRV challenge (contributed by active immunity and passive circulating MatAbs) were consistently (but not significantly) lower in the MatAb-AttHRV/VLP groups than in the corresponding groups without MatAbs. Intestinal B-cell responses in the MatAb-AttHRV/VLP group were most suppressed with significantly reduced or no intestinal immunoglobulin A (IgA) and IgG effector and memory B-cell responses or antibody titers pre- and postchallenge. This suppression was not alleviated but was enhanced after extending vaccination/challenge from 28 to 42 days. In pigs vaccinated with nonreplicating VLP alone that failed to induce protection, MatAb effects differed, with intestinal and systemic IgG ASCs and prechallenge memory B cells suppressed but the low intestinal IgA and IgM ASC responses unaffected. Thus, we demonstrate that MatAbs differentially affect both replicating and nonreplicating HRV vaccines and suggest mechanisms of MatAb interference. This information should facilitate vaccine design to overcome MatAb suppression.

scholarly journals The presence of circulating antibody secreting cells and long-lived memory B cell responses to reticulocyte binding protein 1a in Plasmodium vivax patients

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Piyawan Kochayoo ◽  
Pattarawan Sanguansuttikul ◽  
Pongsakorn Thawornpan ◽  
Kittikorn Wangriatisak ◽  
John H. Adams ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Memory B Cells ◽  
Antibody Responses ◽  
Blood Stage ◽  
Memory B Cell ◽  
Cell Responses ◽  
Antibody Titers ◽  
B Cell Responses

Abstract Background Development of an effective vaccine against blood-stage malaria requires the induction of long-term immune responses. Plasmodium vivax Reticulocyte Binding Protein 1a (PvRBP1a) is a blood-stage parasite antigen which is associated with invasion of red blood cells and induces antibody responses. Thus, PvRBP1a is considered as a target for design of a blood-stage vaccine against vivax malaria. Methods Both cross-sectional and cohort studies were used to explore the development and persistence of long-lived antibody and memory B cell responses to PvRBP1a in individuals who lived in an area of low malaria endemicity. Antibody titers and frequency of memory B cells specific to PvRBP1a were measured during infection and following recovery for up to 12 months. Results IgG antibody responses against PvRBP1a were prevalent during acute vivax malaria, predominantly IgG1 subclass responses. High responders to PvRBP1a had persistent antibody responses for at least 12-month post-infection. Further analysis of high responder found a direct relation between antibody titers and frequency of activated and atypical memory B cells. Furthermore, circulating antibody secreting cells and memory B cells specific to PvRBP1a were generated during infection. The PvRBP1a-specific memory B cells were maintained for up to 3-year post-infection, indicating the ability of PvRBP1a to induce long-term humoral immunity. Conclusion The study revealed an ability of PvRBP1a protein to induce the generation and maintenance of antibody and memory B cell responses. Therefore, PvRBP1a could be considered as a vaccine candidate against the blood-stage of P. vivax.

scholarly journals Distribution of rotavirus-specific memory B cells in gut-associated lymphoid tissue after primary immunization

2001 ◽  
Vol 82 (9) ◽  
pp. 2271-2274 ◽  
Author(s):  
Charlotte A. Moser ◽  
Paul A. Offit
Keyword(s):  
B Cells ◽  
B Cell ◽  
Memory B Cells ◽  
Lymphoid Tissues ◽  
Memory B Cell ◽  
Cell Responses ◽  
Delayed Onset ◽  
Specific Memory ◽  
Small Intestinal ◽  
B Cell Responses

We found previously that mice inoculated orally with simian rotavirus strain RRV developed virus-specific memory B cell responses 16 weeks after immunization that were greater than those found 6 weeks after immunization. Memory B cell responses were defined as the quantity of virus-specific IgA detected in small intestinal lamina propria (LP) fragment cultures of immunized mice at various intervals after challenge. Enhanced memory B cell responses correlated with enhanced protection against shedding. In order to understand better the delayed onset of rotavirus-specific memory B cell responses, a method was developed to determine the frequencies of rotavirus-specific memory B cells in gut-associated lymphoid tissues (GALT). We found that protection against rotavirus challenge was determined by the frequency of rotavirus-specific memory B cells in GALT LP.

scholarly journals Analysis of Memory B-Cell Responses Reveals Suboptimal Dosing Schedule of a Licensed Vaccine

2017 ◽  
Vol 217 (4) ◽  
pp. 572-580 ◽  
Author(s):  
Erin M Scherer ◽  
Robin A Smith ◽  
Joseph J Carter ◽  
Gregory C Wipf ◽  
Daniel F Gallego ◽  
...  
Keyword(s):  
B Cell ◽  
Dosing Schedule ◽  
Memory B Cell ◽  
Cell Responses ◽  
B Cell Responses

scholarly journals SARS‐CoV‐2 sculpts the immune system to induce sustained virus‐specific naïve‐like and memory B‐cell responses

2021 ◽  
Vol 10 (9) ◽  
Author(s):  
Leire de Campos‐Mata ◽  
Sonia Tejedor Vaquero ◽  
Roser Tachó‐Piñot ◽  
Janet Piñero ◽  
Emilie K Grasset ◽  
...  
Keyword(s):  
Immune System ◽  
B Cell ◽  
Memory B Cell ◽  
Cell Responses ◽  
B Cell Responses

Memory B cell responses following immunisation with polysaccharide and conjugate quadrivalent meningococcal ACYW135 vaccines in healthy adult volunteers

2010 ◽  
Vol 61 (6) ◽  
pp. 517
Author(s):  
Maheshi Ramasamy ◽  
Elizabeth Clutterbuck ◽  
Jaclyn Bowman ◽  
Matthew D. Snape ◽  
Mushiya Mpelembue ◽  
...  
Keyword(s):  
B Cell ◽  
Healthy Adult ◽  
Memory B Cell ◽  
Cell Responses ◽  
B Cell Responses ◽  
Adult Volunteers

scholarly journals The acquisition of long-lived memory B cell responses to merozoite surface protein-8 in individuals with Plasmodium vivax infection

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Piyawan Kochayoo ◽  
Natthapon Kittisenachai ◽  
Siriruk Changrob ◽  
Kittikorn Wangriatisak ◽  
Fauzi Muh ◽  
...  
Keyword(s):  
B Cell ◽  
Plasmodium Vivax ◽  
Surface Protein ◽  
Merozoite Surface Protein ◽  
Vivax Infection ◽  
Memory B Cell ◽  
Cell Responses ◽  
B Cell Responses

Agonist for Toll-Like Receptor (TLR) 9 Amplifies as Well as Inhibits the Differentiation of FVIII-Specific Memory B Cells into Antibody-Producing Plasma Cells in Vitro and in Vivo.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3382-3382
Author(s):  
Peter Allacher ◽  
Christina Hausl ◽  
Aniko Ginta Pordes ◽  
Rafi Uddin Ahmad ◽  
Hartmut J Ehrlich ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Memory B Cells ◽  
Memory B Cell ◽  
Cpg Dna ◽  
Cell Responses ◽  
Specific Memory ◽  
B Cell Responses

Abstract Memory B cells are essential for maintaining long-term antibody responses. They can persist for years even in the absence of antigen and are rapidly re-stimulated to differentiate into antibody-producing plasma cells when they encounter their specific antigen. Previously we demonstrated that ligands for TLR 7 and 9 amplify the differentiation of FVIII-specific memory B cells into anti-FVIII antibody-producing plasma cells at low concentrations of FVIII and prevent the inhibition of memory-B-cell differentiation at high concentrations of FVIII. The modulation of FVIII-specific memory-B-cell responses by agonists for TLR is highly relevant for the design of new immunotherapeutic approaches in patients with FVIII inhibitors because TLR are activated by a range of different viral and bacterial components. Specifically, TLR 7 is triggered by single-stranded RNA derived from viruses and TLR 9 is triggered by bacterial DNA containing unmethylated CpG motifs. We further explored the modulation of FVIII-specific memory-B-cell responses by agonists for TLRs by studying a broad range of concentrations of CpG DNA, a ligand for TLR 9, both in vitro and in vivo using the murine E17 model of hemophilia A. We used CpG-DNA in concentrations ranging from 0.1 to 10,000 ng/ml to study the modulation of FVIII-specific memory-B-cell responses in vitro and verified the specificity of the effects observed by including a blocking agent for TLR 9 and GpC-DNA, a non-stimulating negative control for CpG DNA. Furthermore, we used doses of CpG DNA ranging from 10 to 50,000 ng per dose to study the modulation of FVIII-specific memory-B-cell responses in vivo. E17 hemophilic mice were treated with a single intravenous dose of 200 ng FVIII to stimulate the generation of FVIII-specific memory B cells and were subsequently treated with another dose of FVIII that was given together with CpG DNA. We analyzed titers of anti-FVIII antibodies in the circulation of these mice one week after the second dose of FVIII. Previously we had shown that a single dose of 200 ng FVIII, given intravenously to E17 hemophilic mice, stimulates the formation of FVIII-specific memory B cells but is not sufficient to induce anti-FVIII antibodies that would be detectable in the circulation. Our results demonstrate a biphasic effect of CpG DNA on the re-stimulation of FVIII-specific memory B cells and their differentiation into antibody-producing plasma cells. Both in vitro and in vivo studies show that CpG DNA at high doses inhibits the re-stimulation and differentiation of FVIII-specific memory B cells. However, CpG DNA at low doses amplifies these processes. Amplification and inhibition of memory-B-cell responses are due to specific interactions of CpG DNA with TLR 9. Both effects are blocked by addition of a blocking agent for TLR 9 in vitro. We conclude that triggering of TLR 9 by bacterial DNA has a substantial influence on FVIII-specific memory-B-cell responses. The consequence of TLR 9 triggering can be inhibitory or stimulatory, depending on the actual concentration of the bacterial DNA. Our findings demonstrate the potential modulatory effects of bacterial infections on the regulation of FVIII inhibitor development.

Sign in / Sign up

Export Citation Format

Share Document