Identification of B-Cell Subsets

Tung, James W.; Parks, David R.; Moore, Wayne A.; Herzenberg, Leonard A.; Herzenberg, Leonore A.

doi:10.1385/1-59259-796-3:037

Cited by 29 publications

(27 citation statements)

References 20 publications

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“…Since the spleen is an important organ where B cell development takes place, to further examine different B cell subpopulations, the numbers and percentages of T1-newly formed B (T1- (29,30).…”

Section: Coinfection Reduced Both the Numbers And Percentages Of B Cementioning

confidence: 99%

Lethal Coinfection of Influenza Virus and Streptococcus pneumoniae Lowers Antibody Response to Influenza Virus in Lung and Reduces Numbers of Germinal Center B Cells, T Follicular Helper Cells, and Plasma Cells in Mediastinal Lymph Node

Lam

et al. 2015

J Virol

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Secondary Streptococcus pneumoniae infection after influenza is a significant clinical complication resulting in morbidity and sometimes mortality. Prior influenza virus infection has been demonstrated to impair the macrophage and neutrophil response to the subsequent pneumococcal infection. In contrast, how a secondary pneumococcal infection after influenza can affect the adaptive immune response to the initial influenza virus infection is less well understood. Therefore, this study focuses on how secondary pneumococcal infection after influenza may impact the humoral immune response to the initial influenza virus infection in a lethal coinfection mouse model. Compared to mice infected with influenza virus alone, mice coinfected with influenza virus followed by pneumococcus had significant body weight loss and 100% mortality. S econdary bacterial infection of the respiratory tract following influenza is a severe complication that often increases morbidity (1). Streptococcus pneumoniae is one of the pathogens that commonly cause the coinfection (2). Pneumococcus is also the major pathogen associated with mortality in both the 1918 Spanish influenza pandemic (3-5) and the 2009 H1N1 pandemic (6, 7). Given this clinical importance, it is imperative that we understand how the host immune response can be modulated after the coinfection.Prior influenza virus infection has been demonstrated to impair the immune defense against subsequent pneumococcal growth and infection (8, 9). For example, influenza virus can desensitize epithelial cells and alveolar macrophages to Toll-like receptor (TLR) signals for defense against bacteria (10). Gamma interferon (IFN-␥) induced by influenza virus can inhibit the phagocytosis of pneumococcus by macrophages (11). The type I IFN induced by influenza virus can impair neutrophils (12) and macrophages (13) in the defense against pneumococcus. Influenza virus can decrease tumor necrosis factor alpha (TNF-␣) production from natural killer cells in the lung, which allows an increase bacterial growth (14).In contrast, how secondary pneumococcal infection after influenza can influence the immune response to the initial influenza virus is relatively less well understood. The host adaptive immune response is largely responsible for controlling the influenza virus infection. It has been reported that coinfection could dysregulate Th17 (15) and gamma/delta T cells (16). However, whether the B cell response would be modulated during the coinfection is still not clear. It is reported that vaccine-induced immunity to influenza virus

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Section: Coinfection Reduced Both the Numbers And Percentages Of B Cementioning

confidence: 99%

Lethal Coinfection of Influenza Virus and Streptococcus pneumoniae Lowers Antibody Response to Influenza Virus in Lung and Reduces Numbers of Germinal Center B Cells, T Follicular Helper Cells, and Plasma Cells in Mediastinal Lymph Node

Lam

et al. 2015

J Virol

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“…They express CD19, low levels of IgD but relatively high levels of IgM. They can express CD43 and CD9, are negative or low expressers for other markers such as CD21 and CD23, and are mostly intermediate for B220 (27, 31, 82–84). In the spleen, many of their characteristics are similar to transitional B-cells when at a transitional T1 stage.…”

Section: The Distinct Flavors Of B-cell Subsetsmentioning

confidence: 99%

B1b Cells Recognize Protective Antigens after Natural Infection and Vaccination

Cunningham¹,

Flores‐Langarica²,

Bobat³

et al. 2014

Front. Immunol.

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There are multiple, distinct B-cell populations in human beings and other animals such as mice. In the latter species, there is a well-characterized subset of B-cells known as B1 cells, which are enriched in peripheral sites such as the peritoneal cavity but are rare in the blood. B1 cells can be further subdivided into B1a and B1b subsets. There may be additional B1 subsets, though it is unclear if these are distinct populations or stages in the developmental process to become mature B1a and B1b cells. A limitation in understanding B1 subsets is the relative paucity of specific surface markers. In contrast to mice, the existence of B1 cells in human beings is controversial and more studies are needed to investigate the nature of these enigmatic cells. Examples of B1b antigens include pneumococcal polysaccharide and the Vi antigen from Salmonella Typhi, both used routinely as vaccines in human beings and experimental antigens such as haptenated-Ficoll. In addition to inducing classical T-dependent responses some proteins are B1b antigens and can induce T-independent (TI) immunity, examples include factor H binding protein from Borrelia hermsii and porins from Salmonella. Therefore, B1b antigens can be proteinaceous or non-proteinaceous, induce TI responses, memory, and immunity, they exist in a diverse range of pathogenic bacteria, and a single species can contain multiple B1b antigens. An unexpected benefit to studying B1b cells is that they appear to have a propensity to recognize protective antigens in bacteria. This suggests that studying B1b cells may be rewarding for vaccine design as immunoprophylactic and immunotherapeutic interventions become more important due to the decreasing efficacy of small molecule antimicrobials.

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“…Although this determinant is readily detectable on mature B-1 cells, it is usually expressed at lower levels on these cells than on B-2 cells (18,19). In fact, the B220-6B2 monoclonal antibody was adopted for general use for B cell identification in our laboratory (and elsewhere) specifically because, although its expression overlaps on B-1 and B-2 cells, it provides an opportunity to estimate whether B-1 or B-2 cells predominate in a given B cell population (18).…”

Section: Cd138 Expression As a Marker For B Lineage Progenitorsmentioning

confidence: 99%

Phenotypically distinct B cell development pathways map to the three B cell lineages in the mouse

Tung

Mrazek

Yang

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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130

103

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B-1 cells ͉ B-2 cells ͉ CD138 ͉ MHC class II ͉ progenitors S ome time ago, our laboratory proposed the existence of three B lymphocyte lineages (B-1a, B-1b, and B-2) in the mouse (1-3). We based this proposal on in vivo reconstitution studies demonstrating that progenitors for these lineages are enriched differentially in traditional sites for lymphocyte progenitors, i.e., B-1a progenitors are found principally in fetal liver, neonatal spleen, and neonatal bone marrow (BM), whereas B-1b and B-2 progenitors are found principally in adult BM. In the ensuing years, alternate theories were advanced suggesting that antigendriven differentiation of mature B cells accounted for the development of these functionally distinct B cells subsets (4-9). However, in a recent paper, directly demonstrate that B-1a, B-1b, and B-2 belong to three separate lineages by showing that they derive from phenotypically and temporally distinct progenitors, i.e., progenitors for B-2 cells are phenotypically distinct from progenitors for B-1a and B-1b; among progenitors for B-1 cells, B-1a progenitors are found principally in neonates, whereas progenitors for B-1b are found principally in adults.Studies here provide key support for the existence of the distinct B cell lineages by showing that the predominant B cell development pathway in adults, where B-2 development predominates, is phenotypically distinct from the predominant pathway in neonates, where B-1 development predominates. In essence, we show that syndecan-1 (CD138) and MHC class II (I-A) are both expressed throughout B cell development in the predominant B cell pathway adult BM, beginning when Ig rearrangement is initiated [at Hardy fraction (Fr.) B (11)] and persisting thereafter (I-A), or terminating when the B cells reach maturity (CD138). In contrast, neither marker is expressed during early B cell development in the predominant pathway in neonatal BM and spleen, where I-A appears initially on mature B cells (12, 13), and CD138 is not detectable on most of the developing B cells.

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Identification of B-Cell Subsets

Cited by 29 publications

References 20 publications

Lethal Coinfection of Influenza Virus and Streptococcus pneumoniae Lowers Antibody Response to Influenza Virus in Lung and Reduces Numbers of Germinal Center B Cells, T Follicular Helper Cells, and Plasma Cells in Mediastinal Lymph Node

Lethal Coinfection of Influenza Virus and Streptococcus pneumoniae Lowers Antibody Response to Influenza Virus in Lung and Reduces Numbers of Germinal Center B Cells, T Follicular Helper Cells, and Plasma Cells in Mediastinal Lymph Node

B1b Cells Recognize Protective Antigens after Natural Infection and Vaccination

Phenotypically distinct B cell development pathways map to the three B cell lineages in the mouse

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