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The toll-like receptor protein RP105 regulates lipopolysaccharide signaling in B cells.

Ogata H, Su I, Miyake K, Nagai Y, Akashi S, Mecklenbräuker I, Rajewsky K, Kimoto M, Tarakhovsky A - J. Exp. Med. (2000)

Bottom Line: Here, we demonstrate that the responses of B cells to LPS are also regulated by another TLR protein, RP105, which is predominantly expressed on mature B cells in mice and humans.Using originally LPS-unresponsive Ba/F3 cells expressing exogenous TLR4 and RP105, we demonstrate the functional cooperation between TLR4 and RP105 in LPS-induced nuclear factor kappaB activation.These data suggest the existence of the TLR4-RP105 signaling module in the LPS-induced B cell activation.

View Article: PubMed Central - PubMed

Affiliation: Department of Immunology, Saga Medical School, Saga 849-8501, Japan.

ABSTRACT
The susceptibility to infections induced by Gram-negative bacteria is largely determined by innate immune responses to bacteria cell wall lipopolysaccharide (LPS). The stimulation of B cells by LPS enhances their antigen-presenting capacity and is accompanied by B cell proliferation and secretion of large quantities of LPS-neutralizing antibodies. Similar to macrophages and neutrophils, the LPS-induced activation of B cells is dependent on Toll-like receptor (TLR)4. Here, we demonstrate that the responses of B cells to LPS are also regulated by another TLR protein, RP105, which is predominantly expressed on mature B cells in mice and humans. The analysis of mice homozygous for the mutation in the RP105 gene revealed impaired proliferative and humoral immune responses of RP105-deficient B cells to LPS. Using originally LPS-unresponsive Ba/F3 cells expressing exogenous TLR4 and RP105, we demonstrate the functional cooperation between TLR4 and RP105 in LPS-induced nuclear factor kappaB activation. These data suggest the existence of the TLR4-RP105 signaling module in the LPS-induced B cell activation.

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B lymphocyte populations in RP105-deficient mice. Flow cytometric analysis of bone marrow cells, splenocytes, thymocytes, and peritoneal cavity cells in 8-wk-old wild-type C57BL/6 and RP105-deficient mice. Numbers indicate the fraction (%) of gated cellular subpopulations within the lymphocyte population.
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Figure 2: B lymphocyte populations in RP105-deficient mice. Flow cytometric analysis of bone marrow cells, splenocytes, thymocytes, and peritoneal cavity cells in 8-wk-old wild-type C57BL/6 and RP105-deficient mice. Numbers indicate the fraction (%) of gated cellular subpopulations within the lymphocyte population.

Mentions: The flow cytometric analyses and absolute numbers of the bone marrow cells, splenocytes, lymph nodes, and peritoneal cells derived from RP105-deficient mice did not reveal changes in sizes of developing and mature B cell subpopulations compared with the control wild-type mice (Fig. 2; Table ). These data exclude the significant role of RP105 in B cell development.


The toll-like receptor protein RP105 regulates lipopolysaccharide signaling in B cells.

Ogata H, Su I, Miyake K, Nagai Y, Akashi S, Mecklenbräuker I, Rajewsky K, Kimoto M, Tarakhovsky A - J. Exp. Med. (2000)

B lymphocyte populations in RP105-deficient mice. Flow cytometric analysis of bone marrow cells, splenocytes, thymocytes, and peritoneal cavity cells in 8-wk-old wild-type C57BL/6 and RP105-deficient mice. Numbers indicate the fraction (%) of gated cellular subpopulations within the lymphocyte population.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC1887709&req=5

Figure 2: B lymphocyte populations in RP105-deficient mice. Flow cytometric analysis of bone marrow cells, splenocytes, thymocytes, and peritoneal cavity cells in 8-wk-old wild-type C57BL/6 and RP105-deficient mice. Numbers indicate the fraction (%) of gated cellular subpopulations within the lymphocyte population.
Mentions: The flow cytometric analyses and absolute numbers of the bone marrow cells, splenocytes, lymph nodes, and peritoneal cells derived from RP105-deficient mice did not reveal changes in sizes of developing and mature B cell subpopulations compared with the control wild-type mice (Fig. 2; Table ). These data exclude the significant role of RP105 in B cell development.

Bottom Line: Here, we demonstrate that the responses of B cells to LPS are also regulated by another TLR protein, RP105, which is predominantly expressed on mature B cells in mice and humans.Using originally LPS-unresponsive Ba/F3 cells expressing exogenous TLR4 and RP105, we demonstrate the functional cooperation between TLR4 and RP105 in LPS-induced nuclear factor kappaB activation.These data suggest the existence of the TLR4-RP105 signaling module in the LPS-induced B cell activation.

View Article: PubMed Central - PubMed

Affiliation: Department of Immunology, Saga Medical School, Saga 849-8501, Japan.

ABSTRACT
The susceptibility to infections induced by Gram-negative bacteria is largely determined by innate immune responses to bacteria cell wall lipopolysaccharide (LPS). The stimulation of B cells by LPS enhances their antigen-presenting capacity and is accompanied by B cell proliferation and secretion of large quantities of LPS-neutralizing antibodies. Similar to macrophages and neutrophils, the LPS-induced activation of B cells is dependent on Toll-like receptor (TLR)4. Here, we demonstrate that the responses of B cells to LPS are also regulated by another TLR protein, RP105, which is predominantly expressed on mature B cells in mice and humans. The analysis of mice homozygous for the mutation in the RP105 gene revealed impaired proliferative and humoral immune responses of RP105-deficient B cells to LPS. Using originally LPS-unresponsive Ba/F3 cells expressing exogenous TLR4 and RP105, we demonstrate the functional cooperation between TLR4 and RP105 in LPS-induced nuclear factor kappaB activation. These data suggest the existence of the TLR4-RP105 signaling module in the LPS-induced B cell activation.

Show MeSH
Related in: MedlinePlus