λ5 is required for rearrangement of the Ig κ light chain gene in pro-B cell lines

Miyazaki, Takahiro; Kato, Ibuki; Takeshita, Satoshi; Karasuyama, Hajime; Kudo, Akira

doi:10.1093/intimm/11.8.1195

Cited by 15 publications

(15 citation statements)

References 28 publications

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“…4C, Tumor-1 did not show an increased expression of ganp gene, whereas most of the tumor lines showed higher levels of ganp transcripts. Tumor-1 showed distinct oligoclonal configurations of (35,36) and were also used in the mutation analysis is of the sequences. The J regions of heavy and light chains were estimated by the sizes of the bands hybridized with the probes onto the blots of PCR analysis for Ig gene rearrangement of genomic DNAs.…”

Section: Discussionmentioning

confidence: 99%

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Increased Expression of Germinal Center–Associated Nuclear Protein RNA-Primase Is Associated with Lymphomagenesis

Fujimura

Xing

Takeya³

et al. 2005

Cancer Research

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Lymphomas arise containing abnormalities of various differentiation stage-specific molecules. In the study reported here, we have shown abnormal up-regulation of germinal center B cell-associated GANP in various human lymphomas including mantle cell, diffuse large B cell, and Hodgkin lymphoma, by immunohistochemical analysis. To study the role of GANP in lymphomagenesis, we generated mutant mice (ganp-Tg) that express the transgenic ganp gene under immunoglobulin enhancer and promoter control. Ganp-Tg mice showed a high incidence of lymphomagenesis (29.5%) after aging with a non-B/non-T cell surface phenotype having slight CD45R/B220 expression and Ig transcripts of rearranged VH-DH-JH IgH loci. Lymphomas generated in ganp-Tg mice displayed similar pathologic characteristics to mouse reticulum cell neoplasm or Hodgkin lymphoma-like lesions. The VH sequences of individual mice showed that the tumors proliferated from a single clone or oligoclones, as is found in human diffuse large B-cell lymphomas and Hodgkin lymphoma. These results suggest that GANP overexpression is a causative factor in the generation of B lymphomas. (Cancer Res 2005; 65(13): 5925-34)

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Section: Discussionmentioning

confidence: 99%

“…Primers for mouse Vj genes were described previously (36): Vjcon (5V-GGCTGCAGSTTCAGTGG-CAGTGGRTCWGGRAC-3V) and Jj5 (5V-TGCCACGTCAACTGATAAT-GAGCCCTCTC-3V).…”

Section: Methodsmentioning

confidence: 99%

Increased Expression of Germinal Center–Associated Nuclear Protein RNA-Primase Is Associated with Lymphomagenesis

Fujimura

Xing

Takeya³

et al. 2005

Cancer Research

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“…Pro-B cells derived from bone marrow cells of BALB/c mice and Fc␥RIIB-deficient mice were cultured with the mouse stromal cell line, ST2 (a gift of Dr. Nishikawa, Kyoto University, Kyoto Japan), in the presence of IL-7 as described previously (10). PreBR and Fc␥ Ϫ/Ϫ PreBR cell lines were established from pro-B cells in the presence of IL-7 after removal of ST2 as described previously (35).…”

Section: Animals and Cell Linesmentioning

confidence: 99%

“…FITC-conjugated streptavidin was purchased from Cosmo Bio (Tokyo, Japan). Flow cytometric analyses using the FACSCalibur (BD Biosciences, Mountain View, CA) were performed as described (10).…”

Section: Abs and Flow Cytometric Analysesmentioning

confidence: 99%

“…There were almost no mature B cells in bone marrow, indicating that a more severe B cell deficiency is caused by loss of 5 expression in humans than in mice (9). Recently, we observed that the SL chain activated the -chain rearrangement by restoration of 5 to 5-deficient pro-B cell lines (10). These results indicate that in mice and humans with 5 mutations, B cell differentiation is impaired at the transition from the pro-B/pre-BI to the pre-BII cell stage, during which Ig L chain gene rearrangement takes place.…”

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confidence: 96%

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The Pre-B Cell Receptor Signaling for Apoptosis Is Negatively Regulated by FcγRIIB

Kato

Takai

Kudo

2002

The Journal of Immunology

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Many studies have shown that FcγRIIB is a negative regulator of B cell receptor signaling, and even though FcγRIIB is expressed through all developmental stages of the B cell lineage, its involvement in pre-B cell receptor (pre-BCR) signaling has not been examined. To investigate FcγRIIB function at the pre-B cell stage, we have established pre-BCR positive pre-B cell lines from normal mice and FcγRIIB-deficient mice, named PreBR and Fcγ−/−PreBR, respectively. These cell lines are able to differentiate into immature B cells in vitro by removal of IL-7. In PreBR, apoptosis was moderately induced by F(ab′)2 anti-μ Ab, but not by intact anti-μ Ab. Phosphorylation of SH2-containing inositol 5-phosphatase (SHIP) and Dok, which are involved in FcγRIIB signaling, was induced by anti-μ cross-linking in PreBR. In contrast, apoptosis was strongly induced by both the F(ab′)2 and intact anti-μ Abs in Fcγ−/−PreBR, and the level of phosphorylation of SHIP or Dok was much lower in Fcγ−/−PreBR than those observed in PreBR. Restoration of FcγRIIB to Fcγ−/−PreBR followed by anti-μ cross-linking blocked severe apoptosis, and up-regulated SHIP and Dok phosphorylation. The results demonstrate that FcγRIIB negatively regulates pre-BCR-mediated signaling for apoptosis.

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TRANCE together with IL‐7 induces pre‐B cells to proliferate

Kato¹,

Sato²,

Kudo³

2003

Eur J Immunol

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TRANCE (TNF-related activation-induced cytokine)-deficient mice completely lack osteoclasts, and develop severe osteopetrosis. These mice also show a defect in their pre-B cell differentiation. In the present study, the expression of TRANCE was examined in pre-B cell lines using flow cytometry and reverse transcription-PCR. Three pre-B cell lines, 18-81, B 3 P 8 16-1, and 38B9, expressed TRANCE on their surface, and two pre-B cell lines, 70Z/3 and NFS5, at the late pre-B cell stage, expressed it at low levels, although their mRNA expression was normal. Another pre-B cell line, 38-C-13, at the intermediate stage between pre-B and immature B cells, did not express TRANCE. The IL-7-dependent pre-B cell line PreBR, which expresses the pre-B cell receptor on the cell surface, also expressed TRANCE. When differentiation of PreBR cells was induced in vitro by removing IL-7 from cultures, TRANCE expression dropped; it was restored by the addition of IL-7, suggesting that TRANCE functions in cooperation with IL-7. To examine the function of TRANCE, we introduced the TRANCE gene into PreBR cells and established two transfectants that constitutively expressed TRANCE, even in the absence of IL-7. In these transfectants, after removal of IL-7, the number of cells that succeeded in ‹ chain rearrangement was decreased to one third; and CD40 expression decreased to less than one tenth. Moreover, the percentage of cells in the S/G2/M phase was increased by 50% over the mock transfectant. These findings indicate that, before ‹ chain rearrangement occurs, TRANCE together with IL-7 induces pre-B cells to proliferate and makes this rearrangement more efficient.

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λ5 is required for rearrangement of the Ig κ light chain gene in pro-B cell lines

Cited by 15 publications

References 28 publications

Increased Expression of Germinal Center–Associated Nuclear Protein RNA-Primase Is Associated with Lymphomagenesis

Increased Expression of Germinal Center–Associated Nuclear Protein RNA-Primase Is Associated with Lymphomagenesis

The Pre-B Cell Receptor Signaling for Apoptosis Is Negatively Regulated by FcγRIIB

TRANCE together with IL‐7 induces pre‐B cells to proliferate

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