Detection of memory B lymphocytes specific to hepatitis B virus (HBV) surface antigen (HBsAg) from HBsAg-vaccinated or HBV-immunized subjects by ELISPOT assay

Tuaillon, Édouard; Tabaa, Yassine Al; Petitjean, Gaël; Huguet, Marie-France; Pajeaux, Georges; Fondere, Jean-Michel; Ponseille, Benoît; Ducos, J; Blanc, Pierre; Vendrell, Jean-François

doi:10.1016/j.jim.2006.07.016

Cited by 55 publications

(48 citation statements)

References 38 publications

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“…However, as will be repeatedly emphasized in this article, the immune system has evolved to be redundant, and vaccines, like prior natural infection, may protect through multiple mechanisms. (iv) Memory induced by vaccination may be crucial to protection, particularly in long-incubation diseases, such as hepatitis B (86,185). Although loss of antibody after vaccination may render vaccinees again susceptible to some infections (90), central memory established by vaccination is sufficient under certain circumstances to confer protection (20).…”

Section: General Principlesmentioning

confidence: 99%

“…Antibody tests often become negative years after hepatitis B vaccination, yet protection appears to be solid and long-lasting, and no booster vaccination is recommended (30,185,188,193). Postvaccination titers of 10 mIU/ml or greater correlate with the induction of the T helper cell responses that mediate the memory of B cells.…”

Section: Hepatitis Virusesmentioning

confidence: 99%

“…Postvaccination titers of 10 mIU/ml or greater correlate with the induction of the T helper cell responses that mediate the memory of B cells. Thus, when the vaccinee is exposed to hepatitis B virus, there is an anamnestic response that prevents disease, and often infection as well (23,30,48,64,108,178,185,187). In a study of children vaccinated 5 to 7 years previously, 46% had antibody titers below 10 mIU/ml.…”

Section: Hepatitis Virusesmentioning

confidence: 99%

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Correlates of Protection Induced by Vaccination

Plotkin

2010

Clin Vaccine Immunol

1,477

1,158

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This paper attempts to summarize current knowledge about immune responses to vaccines that correlate with protection. Although the immune system is redundant, almost all current vaccines work through antibodies in serum or on mucosa that block infection or bacteremia/viremia and thus provide a correlate of protection. The functional characteristics of antibodies, as well as quantity, are important. Antibody may be highly correlated with protection or synergistic with other functions. Immune memory is a critical correlate: effector memory for short-incubation diseases and central memory for long-incubation diseases. Cellular immunity acts to kill or suppress intracellular pathogens and may also synergize with antibody. For some vaccines, we have no true correlates, but only useful surrogates, for an unknown protective response.

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Section: General Principlesmentioning

confidence: 99%

Section: Hepatitis Virusesmentioning

confidence: 99%

Section: Hepatitis Virusesmentioning

confidence: 99%

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Correlates of Protection Induced by Vaccination

Plotkin

2010

Clin Vaccine Immunol

1,477

1,158

View full text Add to dashboard Cite

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“…It was found that memory B cells generated in normal individuals vaccinated against hepatitis B and HIV-infected patients differentiated into Ag-specific IgM-, IgG-, and IgA-secreting B cells in vitro in response to CD40L, IL-2, and IL-10. The IgM-secreting cells represented ϳ30% of all Ag-specific Ig-secreting cells generated (82,83). Although it could be argued that CD27 Ϫ B cells gave rise to Ag-specific IgM-secreting cells, this is unlikely because Ͻ5% of CD27 Ϫ B cells differentiate into Ig-secreting cells in vitro in response to CD40L, IL-2 and IL-10; this response is dominated by CD27 ϩ B cells (19,21,36,82).…”

Section: Cd27mentioning

confidence: 99%

Human IgM+CD27+ B Cells: Memory B Cells or “Memory” B Cells?

Tangye

Good

2007

The Journal of Immunology

218

200

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Memory B cells are generated in germinal centers (GC) and contribute to serological immunity by rapidly differentiating into plasma cells. Human memory B cells can be identified by the expression of CD27. These cells exhibit more rapid responses than naive (CD27−) B cells following stimulation in vitro, consistent with the heightened kinetics of secondary responses in vivo. CD27+ B cells express mutated Ig V region genes; however a significant proportion continue to express IgM, suggesting the existence of IgM+ memory B cells. The observation that mutated IgM+CD27+ B cells are generated in humans who cannot form GC led to the conclusions that these cells are generated independently of GC and thus are not memory cells and that they mediate responses to T cell-independent Ag. Although some studies support the idea that IgM+CD27+ B cells participate in T cell-independent responses, many others do not. In this review we will provide alternate interpretations of the biology of IgM+CD27+ B cells and propose that they are indeed memory cells.

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“…(19,37,46). IgM antibody has been thought to play a role mainly with T-cell-independent nonprotein antigens that can activate B cells on their own through cross-linking, while switched-memory cells that have interacted with T cells in germinal centers (10,42). The existence of IgM memory cells to CTB after cholera infection is consistent with these observations.…”

Section: Discussionmentioning

confidence: 62%

Development of Immunoglobulin M Memory to Both a T-Cell-Independent and a T-Cell-Dependent Antigen following Infection withVibrio choleraeO1 in Bangladesh

et al. 2010

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Vibrio cholerae O1 can cause severe watery diarrhea that can be life-threatening without treatment. Infection results in long-lasting protection against subsequent disease. Development of memory B cells of the immunoglobulin G (IgG) and IgA isotypes to V. cholerae O1 antigens, including serotype-specific lipopolysaccharide (LPS) and the B subunit of cholera toxin (CTB), after cholera infection has been demonstrated. Memory B cells of the IgM isotype may play a role in long-term protection, particularly against T-cell-independent antigens, but IgM memory has not been studied in V. cholerae O1 infection. Therefore, we assayed acute-and convalescent-phase blood samples from cholera patients for the presence of memory B cells that produce cholera antigen-specific IgM antibody upon polyclonal stimulation in in vitro culture. We also examined the development of serological and antibody-secreting cell responses following infection. Subjects developed significant IgM memory responses by day 30 after infection, both to the T-cell-independent antigen LPS and to the T-cell-dependent antigen CTB. No significant corresponding elevations in plasma IgM antibodies or circulating IgM antibody-secreting cells to CTB were detected. In 17 subjects followed to day 90 after infection, significant persistence of elevated IgM memory responses was not observed. The IgM memory response to CTB was negatively correlated with the IgG plasma antibody response to CTB, and there was a trend toward negative correlation between the IgM memory and IgA plasma antibody responses to LPS. We did not observe an association between the IgM memory response to LPS and the vibriocidal titer.

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Detection of memory B lymphocytes specific to hepatitis B virus (HBV) surface antigen (HBsAg) from HBsAg-vaccinated or HBV-immunized subjects by ELISPOT assay

Cited by 55 publications

References 38 publications

Correlates of Protection Induced by Vaccination

Correlates of Protection Induced by Vaccination

Human IgM+CD27+ B Cells: Memory B Cells or “Memory” B Cells?

Development of Immunoglobulin M Memory to Both a T-Cell-Independent and a T-Cell-Dependent Antigen following Infection withVibrio choleraeO1 in Bangladesh

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