B cell mediated priming following pneumococcal colonization

Rabquer, Bradley J.; Shriner, Anne K.; Smithson, S. Louise; Westerink, M. A. Julie

doi:10.1016/j.vaccine.2006.11.039

Cited by 7 publications

(6 citation statements)

References 25 publications

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“…This may be an indication of an underlying susceptibility to pneumococcal carriage, with elevated serum immunoglobulin indicative of repeated exposure. Although it is well established that repeated exposure to pneumococci is required for the maintenance of IgGsecreting B MEM populations, more recently it has been suggested that exposure during life also enhances the adult immune response to PCV (19). A similar effect has been observed in the United Kingdom, where lack of Haemophilus influenzae type B carriage led to an increased incidence of disease among children who received a single dose of Hib vaccine (20).…”

Section: Levels Of 6bps Igg and Iga In Serum And Nasal Wash Are Not Amentioning

confidence: 86%

Polysaccharide-Specific Memory B Cells Predict Protection against Experimental Human Pneumococcal Carriage

Pennington

Pojar

Mitsi

et al. 2016

Am J Respir Crit Care Med

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Rationale: We have previously demonstrated that experimental pneumococcal carriage enhances immunity and protects healthy adults against carriage reacquisition after rechallenge with a homologous strain.Objectives: To investigate the role of naturally acquired pneumococcal protein and polysaccharide (PS)-specific immunity in protection against carriage acquisition using a heterologous challenge model. Methods:We identified healthy volunteers that were naturally colonized with pneumococcus and, after clearance of their natural carriage episode, challenged them with a heterologous 6B strain. In another cohort of volunteers we assessed 6BPS-specific, PspA-specific, and PspC-specific IgG and IgA plasma and memory B-cell populations before and 7, 14, and 35 days after experimental pneumococcal inoculation.Measurements and Main Results: Heterologous challenge with 6B resulted in 50% carriage among volunteers with previous natural pneumococcal carriage. Protection from carriage was associated with a high number of circulating 6BPS IgG-secreting memory B cells at baseline. There were no associations between protection from carriage and baseline levels of 6BPS IgG in serum or nasal wash, PspA-specific, or PspC-specific memory B cells or plasma cells. In volunteers who did not develop carriage, the number of circulating 6BPS memory B cells decreased and the number of 6BPS plasma cells increased postinoculation.Conclusions: Our data indicate that naturally acquired PS-specific memory B cells, but not levels of circulating IgG at time of pneumococcal exposure, are associated with protection against carriage acquisition.

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Section: Levels Of 6bps Igg and Iga In Serum And Nasal Wash Are Not Amentioning

confidence: 86%

Polysaccharide-Specific Memory B Cells Predict Protection against Experimental Human Pneumococcal Carriage

Pennington

Pojar

Mitsi

et al. 2016

Am J Respir Crit Care Med

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“…Nasopharyngeal carriage of pneumoccoci is known to induce IgG memory in older children and adults. The continued exposure to pneumococci over many years enhances the adult immune response to Pnc7, and it may be necessary to require maintenance of detectable levels of IgG memory (55) This has been demonstrated in mouse models of protection (55,71).…”

Section: Discussionmentioning

confidence: 99%

Serotype-Specific and Age-Dependent Generation of Pneumococcal Polysaccharide-Specific Memory B-Cell and Antibody Responses to Immunization with a Pneumococcal Conjugate Vaccine

Clutterbuck

Hamaluba

et al. 2008

Clin Vaccine Immunol

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“…In mouse models, depletion of IgM-producing B cells results in impaired immune responses against pneumococcal polysaccharide [59]. Furthermore, transplant of B cells and CD4+ T cells from immunized mice into naive recipients can enhance the immune response to PCV13 vaccination [60]. Findings from these studies point to the pivotal role of IgM, especially IgM+ memory B cells, in host immune responses against pneumococcal infections.…”

Section: Introductionmentioning

confidence: 99%

Humoral immune responses to Streptococcus pneumoniae in the setting of HIV-1 infection

Zhang

Wan

et al. 2015

Vaccine

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Streptococcus pneumonia (pneumococcus) remains one of the most commonly identified causes of bacterial infection in the general population, and the risk is 30-100 fold higher in HIV-infected individuals. Both innate and adaptive host immune responses to pneumococcal infection are important against pathogen invasion. Pneumococcal-specific IgA antibody (Ab) is key to control infection at the mucosal sites. Ab responses against pneumococcal infection by B cells can be generated through T cell-dependent or T cell-independent pathways. Depletion of CD4+ T cells is a hallmark of immunodeficiency in HIV infection and this defect also contributes to B cell dysfunction, which predisposes to infections such as the pneumococcus. Two pneumococcal vaccines have been demonstrated to have potential benefits for HIV-infected patients. One is a T cell dependent 13-valent pneumococcal conjugate vaccine (PCV13); the other is a T cell independent 23-valent pneumococcal polysaccharide vaccine (PPV23). However, many questions remain unknown regarding these two vaccines in the clinical setting in HIV disease. Here we review the latest research regarding B cell immune responses against pneumococcal antigens, whether derived from potentially invading pathogens or vaccinations, in the setting of HIV-1 infection.

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B cell mediated priming following pneumococcal colonization

Cited by 7 publications

References 25 publications

Polysaccharide-Specific Memory B Cells Predict Protection against Experimental Human Pneumococcal Carriage

Polysaccharide-Specific Memory B Cells Predict Protection against Experimental Human Pneumococcal Carriage

Serotype-Specific and Age-Dependent Generation of Pneumococcal Polysaccharide-Specific Memory B-Cell and Antibody Responses to Immunization with a Pneumococcal Conjugate Vaccine

Humoral immune responses to Streptococcus pneumoniae in the setting of HIV-1 infection

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