Toll-like receptor 4-mediated signaling regulates IL-7-driven proliferation and differentiation of B-cell precursors

Li, Qian; Han, Dongmei; Wang, Wei; Liu, Xiaoqing; Sun, Xiuyuan; Zhang, Jun; Li, Rong

doi:10.1038/cmi.2013.55

Cited by 10 publications

(7 citation statements)

References 37 publications

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“…While several inflammatory molecules including LPS are known to be activators of B cells at the maturation stage following export to the periphery, recent studies showed that the TLR4 signaling pathway inhibits proliferation of pro-B and pre-B cells, and promotes the differentiation to IgM + immature B cells in BM. 28 , 29 Consistent with previous studies, the suppression of B-cell differentiation in BM was observed 3 days following sub-lethal dosing of LPS treatment (1.0 mg/kg) ( Figure 6C ). When Tg mice were treated, the actual B-cell number in peripheral blood decreased and a significant reduction of B progenitors in BM was observed ( Figure 6C and D).…”

Section: Resultssupporting

confidence: 91%

“… 7 , 40 As far as the impact on B progenitors in BM is concerned, two research groups previously showed that signaling through TLR4 inhibits pro-B and pre-B proliferation, and enhances differentiation to IgM + immature B cells, using different methods. 28 , 29 In our genetically modified mice, STAP-2 displayed synergistic effects on pre-B-cell proliferation with the TLR4 pathway. However, STAP-2 effects did not involve differentiation to IgM + immature B cells.…”

Section: Discussionmentioning

confidence: 83%

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Signal-transducing adaptor protein-2 delays recovery of B lineage lymphocytes during hematopoietic stress

et al. 2020

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Signal-transducing adaptor protein-2 (STAP-2) was discovered as a C-FMS/M-CSFR interacting protein and subsequently found to function as an adaptor of signaling or transcription factors. These include STAT5, MyD88 and IκB kinase in macrophages, mast cells, and T cells. There is additional information about roles for STAP-2 in several types of malignant diseases including chronic myeloid leukemia, however, none have been reported concerning B lineage lymphocytes. We have now exploited gene targeted and transgenic mice to address this lack of knowledge, and demonstrated that STAP-2 is not required under normal, steady-state conditions. However, recovery of B cells following transplantation was augmented in the absence of STAP-2. This appeared to be restricted to cells of B cell lineage with myeloid rebound noted as unremarkable. Furthermore, all hematological parameters were observed to be normal once recovery from transplantation was complete. Furthermore, overexpression of STAP-2, specifically in lymphoid cells, resulted in reduced numbers of late-stage B cell progenitors within the bone marrow. While numbers of mature peripheral B and T cells were unaffected, recovery from sub-lethal irradiation or transplantation was dramatically reduced. Lipopolysaccharide (LPS) normally suppresses B precursor expansion in response to interleukin 7, however, STAP-2 deficiency made these cells more resistant. Preliminary RNA-Seq analyses indicated multiple signaling pathways in B progenitors as STAP-2-dependent. These findings suggest that STAP-2 modulates formation of B lymphocytes in demand conditions. Further study of this adapter protein could reveal ways to speed recovery of humoral immunity following chemotherapy or transplantation.

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Section: Resultssupporting

confidence: 91%

Section: Discussionmentioning

confidence: 83%

Signal-transducing adaptor protein-2 delays recovery of B lineage lymphocytes during hematopoietic stress

et al. 2020

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“…LPS is a major component of the outer membrane of Gram-negative bacteria and has been used in mammals, amphioxus, fish and lamprey for immunological studies 32 33 34 35 . Consistently with these findings, we observed that the expression levels of VLRB and BLNK were upregulated approximately 2.5-fold in lymphocyte-like cells and supraneural myeloid bodies after stimulation with LPS ( Fig.…”

Section: Discussionmentioning

confidence: 99%

Identification and characterisation of the immune response properties of Lampetra japonica BLNK

Han

Liu

Shi

et al. 2016

Sci Rep

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B cell linker protein (BLNK) is a central linker protein involved in B cell signal transduction in jawed vertebrates. In a previous study, we have reported the identification of a BLNK homolog named Lj-BLNK in lampreys. In this study, a 336 bp cDNA fragment encoding the Lj-BLNK Src homology 2 (SH2) domain was cloned into the vector pET-28a(+) and overexpressed in Escherichia coli BL21. The recombinant fragment of Lj-BLNK (rLj-BLNK) was purifiedby His-Bind affinity chromatography, and polyclonal antibodies against rLj-BLNK were raised in male New Zealand rabbits. Fluorescenceactivated cell sorting (FACS) analysisrevealed that Lj-BLNK was expressed in approximately 48% of the lymphocyte-like cells of control lampreys, and a significant increase in Lj-BLNK expression was observed in lampreys stimulated with lipopolysaccharide (LPS). Western blotting analysis showed that variable lymphocyte receptor B (VLRB) and Lj-BLNKwere distributed in the same immune-relevant tissues, and the levels of both were upregulated in supraneural myeloid bodies and lymphocyte-like cells after LPS stimulation. Immunofluorescence demonstrated that Lj-BLNK was localized in VLRB+ lymphocyte-like cells. These results indicate that the Lj-BLNK protein identified in lampreys might play an important role in the VLRB-mediated adaptive immune response.

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“…In addition, it may regulate the differentiation of B cell precursors by facilitating the generation of sIgM + immature B cells [44]. Recently, Li et al [45] confirmed the critical role of TLR4 in the proliferation and differentiation of B cell precursors in TLR4-mutant C3H/HeJ mice and TLR4-intact C3H/HeN mice. LPS-immunized C3H/HeJ mice showed an increase in the number of pro-B and pre-B cells in the bone marrow compared to LPS-immunized C3H/HeN mice.…”

Section: The Effects Of Tlr4 In Promoting the Proliferation Activmentioning

confidence: 99%

The Role of TLR4 on B Cell Activation and Anti-β2GPI Antibody Production in the Antiphospholipid Syndrome

Cheng

Wang

Zhou

2016

Journal of Immunology Research

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High titer of anti-β 2-glycoprotein I antibodies (anti-β 2GPI Ab) plays a pathogenic role in antiphospholipid syndrome (APS). Numerous studies have focused on the pathological mechanism in APS; however, little attention is paid to the immune mechanism of production of anti-β 2GPI antibodies in APS. Our previous study demonstrated that Toll-like receptor 4 (TLR4) plays a vital role in the maturation of bone marrow-derived dendritic cells (BMDCs) from the mice immunized with human β 2-glycoprotein I (β 2GPI). TLR4 is required for the activation of B cells and the production of autoantibody in mice treated with β 2GPI. However, TLR4 provides a third signal for B cell activation and then promotes B cells better receiving signals from both B cell antigen receptor (BCR) and CD40, thus promoting B cell activation, surface molecules expression, anti-β 2GPI Ab production, and cytokines secretion and making B cell functioning like an antigen presenting cell (APC). At the same time, TLR4 also promotes B cells producing antibodies by upregulating the expression of B-cell activating factor (BAFF). In this paper, we aim to review the functions of TLR4 in B cell immune response and antibody production in autoimmune disease APS and try to find a new way for the prevention and treatment of APS.

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Toll-like receptor 4-mediated signaling regulates IL-7-driven proliferation and differentiation of B-cell precursors

Cited by 10 publications

References 37 publications

Signal-transducing adaptor protein-2 delays recovery of B lineage lymphocytes during hematopoietic stress

Signal-transducing adaptor protein-2 delays recovery of B lineage lymphocytes during hematopoietic stress

Identification and characterisation of the immune response properties of Lampetra japonica BLNK

The Role of TLR4 on B Cell Activation and Anti-β2GPI Antibody Production in the Antiphospholipid Syndrome

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