X‐chromosome‐linked immune‐deficient mice have B‐1b cells

Riggs, James E.; Howell, Koko; Matechin, B.; Matlack, Robin; Pennello, Anthony L.; Chiasson, R.

doi:10.1046/j.1365-2567.2003.01624.x

Cited by 18 publications

(20 citation statements)

References 50 publications

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“…Moreover, these populations were differentially affected by splenectomy, which decreased the B-1a lymphocyte population, but not the B-1b cells (15), and by gene targeting of the G␣i2, PD-1, or H chain genes (16 -18). An age-dependent specific increase of the B-1b subpopulation in leaky SCID mice (19) and in xid mice (20) was also previously shown.…”

supporting

confidence: 70%

IL-9-Induced Expansion of B-1b Cells Restores Numbers but Not Function of B-1 Lymphocytes in xid Mice

Knoops

Louahed

Renauld

2004

The Journal of Immunology

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Mice expressing the X-linked immunodeficiency (xid) mutation lack functional Bruton’s tyrosine kinase and were shown to be specifically deficient in peritoneal B-1 lymphocytes. We have previously shown that IL-9, a cytokine produced by TH2 lymphocytes, promotes B-1 cell expansion in vivo. To determine whether IL-9 overexpression might compensate the xid mutation for B-1 lymphocyte development, we crossed xid mice with IL-9-transgenic mice. In this model, IL-9 restored normal numbers of mature peritoneal B-1 cells that all belonged to the CD5− B-1b subset. Despite this normal B-1 lymphocyte number, IL-9 failed to restore classical functions of B-1 cells, namely, the production of natural IgM Abs, the T15 Id Ab response to phosphorylcholine immunization, and the antipolysaccharide humoral response against Streptococcus pneumoniae. By using bromelain-treated RBC, we showed that the antigenic repertoire of these IL-9-induced B-1b lymphocytes was different from the repertoire of classical CD5+ B-1a cells, indicating that the lack of B-1 function by B-1b cells is associated with distinct Ag specificities. Taken together, our data show that B-1b cell development can restore the peritoneal B-1 population in xid mice but that these B-1b cells are functionally distinct from CD5+ B-1a lymphocytes.

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supporting

confidence: 70%

IL-9-Induced Expansion of B-1b Cells Restores Numbers but Not Function of B-1 Lymphocytes in xid Mice

Knoops

Louahed

Renauld

2004

The Journal of Immunology

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“…It was therefore possible that reduced serum IgM in the DN Bright transgenic mice was due to defects in peritoneal B cells. Because Btk-deficient mice fail to develop B1a peritoneal B cells, but can produce B1b and B2 peritoneal B cells (38,39), we therefore hypothesized that DN Bright mice would be deficient in B1a cells. The DN Bright mice, however, not only produced both B1a and B1b cells (Figure 5A), but total numbers of peritoneal cavity B cells were significantly increased (p=0.0486, two-tailed Student’s T test) by approximately 30% in 11 TG mice relative to controls (2.6×10 6 cells versus 2.0×10 6 cells, respectively).…”

Section: Resultsmentioning

confidence: 99%

Transgenic Mice Expressing Dominant-Negative Bright Exhibit Defects in B1 B Cells

Nixon

Ferrell

Miner

et al. 2008

The Journal of Immunology

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The transcription factor Bright up-regulates Ig H chain production from select V region promoters and requires Bright dimerization, Bruton’s tyrosine kinase (Btk), and the Btk substrate, TFII-I, for this activity. Defects in Btk cause X-linked immunodeficiency disease in mice and humans. Btk-deficient mice exhibit decreased serum IgM production, B cell developmental blocks, absence of peritoneal B1 cells, and subnormal immune responses against Ags, including phosphorylcholine, which confer protection against Streptococcus pneumoniae. Transgenic mice expressing dominant-negative Bright share similarities with Btk-deficient mice, including decreased serum IgM, poor anti-phosphorylcholine responses, and slightly reduced numbers of mature B cells. Although dominant-negative Bright mice developed B1 B cells, these were functionally deficient in Ig secretion. These data suggest a mechanistic explanation for the abnormal responses to phosphorylcholine observed in Btk-deficient mice, and indicate that Bright functions in a subset of Btk-dependent pathways in vivo, particularly those responses dominated by B1 B cells.

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“…However, because BALB.xid mice have fewer B1 cells, they cannot significantly recognize TI-2 antigens and, as a result, they produce low amounts of IgA, IgM and IgG3. In fact, the BALB.xid mice did not have any B1a cells (IgM(hi); CD45(lo); CD23-), but B1b lymphocyte subsets (CD11b+) were present, albeit at a lower frequency than that found in their normal counterparts 8 . The levels of IgA and IgE antibodies were the first ones to turn positive after infection (30-45 days after infection) and these remained positive throughout the study period, thereby indicating the importance of IgE and IgA for detecting recent infection in rodents.…”

Section: Discussionmentioning

confidence: 85%

Experimental lagochilascariosis in X-chromosome-linked immunodeficient mice

Freitas

Prudente

Carvalhaes

2009

Rev. Soc. Bras. Med. Trop.

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Lagochilascaris minor is the etiological agent of lagochilascariosis, a disease that affects the neck region and causes exudative abscesses, with eggs, adult parasites and L3/L4 larvae in the purulent exudates. Mice are now considered to be intermediate hosts for the parasite. To determine the pattern of infection in B1 cell-deficient mice, experimental lagochilascariosis was studied in BALB/c and X-chromosome-linked immunodeficient (xid) mice. BALB.xid-infected mice showed lower numbers of larvae. Third-stage larvae, fourth-stage larvae and adult parasites were found in both strains. BALB/c mice produced IgM, IgG, IgA and IgE against the crude extract and secreted/excreted antigens of the parasite. On the other hand, BALB.xid mice did not produce IgM and produced lower levels of IgG and IgA, and similar quantities of IgE.

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X‐chromosome‐linked immune‐deficient mice have B‐1b cells

Cited by 18 publications

References 50 publications

IL-9-Induced Expansion of B-1b Cells Restores Numbers but Not Function of B-1 Lymphocytes in xid Mice

IL-9-Induced Expansion of B-1b Cells Restores Numbers but Not Function of B-1 Lymphocytes in xid Mice

Transgenic Mice Expressing Dominant-Negative Bright Exhibit Defects in B1 B Cells

Experimental lagochilascariosis in X-chromosome-linked immunodeficient mice

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