Abstract:
:IL-5 preferentially activates B1 cells to produce natural antibodies cross-reactive to self antigens. To determine the role of IL-5 in antibody-mediated autoimmune disease, we generated systemic lupus erythematosus (SLE)-prone (NZB x NZW)F1 mice congenic for IL-5 transgene (TG-F1). The transgene unexpectedly reduced the incidence of lupus nephritis. Anti-DNA antibodies in sera and those produced by splenic B cells in vitro were markedly decreased in TG-F1 mice, while total polyclonal Ig levels were comparable to those in IL-5 transgene-negative (NZB x NZW)F1 (non-TG-F1) littermates. Flow cytometry-sorted splenic B1 cells showed a significant reduction of anti-DNA antibody synthesis in response to IL-5, while proliferative responses to IL-5 did not significantly differ between TG-F1 and non-TG-F1 mice. As TG-F1 mice aged, frequencies of peripheral B1 cells progressively increased, and the mice frequently developed B cell chronic lymphocytic leukemia (B-CLL). Our results suggest that dysregulated, continuous high expression of IL-5 in SLE-prone mice may directly or indirectly mediate a skewed signaling of proliferation/differentiation of self-antigen-activated B1 cells, leading to suppression of autoimmune disease, but instead to aberrant expansion of B1 cells, giving rise to B-CLL. Thus, this model may provide a clue to the pathogenesis of both SLE and B-CLL.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Wen X,Zhang D,Kikuchi Y,Jiang Y,Nakamura K,Xiu Y,Tsurui H,Takahashi K,Abe M,Ohtsuji M,Nishimura H,Takatsu K,Shirai T,Hirose Sdoi
10.1002/eji.200425267keywords:
subject
Has Abstractpub_date
2004-10-01 00:00:00pages
2740-9issue
10eissn
0014-2980issn
1521-4141journal_volume
34pub_type
杂志文章abstract::T helper cell type 2 (Th2) cells when triggered by antibodies to CD3 acquire the capacity to stimulate the polyclonal proliferation of syngeneic, resting B cells. Here, we tested the ability of various monoclonal antibodies (mAb) to block the B cell proliferation-inducing potential of such activated Th2 cells. We demo...
journal_title:European journal of immunology
pub_type: 杂志文章
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journal_title:European journal of immunology
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journal_title:European journal of immunology
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journal_title:European journal of immunology
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journal_title:European journal of immunology
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journal_title:European journal of immunology
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journal_title:European journal of immunology
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doi:10.1002/eji.1830111113
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journal_title:European journal of immunology
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journal_title:European journal of immunology
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journal_title:European journal of immunology
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journal_title:European journal of immunology
pub_type: 评论,杂志文章
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journal_title:European journal of immunology
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journal_title:European journal of immunology
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journal_title:European journal of immunology
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journal_title:European journal of immunology
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journal_title:European journal of immunology
pub_type: 杂志文章
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journal_title:European journal of immunology
pub_type: 杂志文章
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journal_title:European journal of immunology
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