CpG inhibits pro-B cell expansion through a cathepsin B-dependent mechanism

Ana Inés Lalanne; Ignacio Moraga; Yi Hao; João Pedro Pereira; Nuno L. Alves; Nicholas D. Huntington; Antonio A. Freitas; Ana Cumano; Paulo Vieira

doi:10.4049/jimmunol.0903854

CpG inhibits pro-B cell expansion through a cathepsin B-dependent mechanism

Ana Inés Lalanne, Ignacio Moraga, Yi Hao, João Pedro Pereira, Nuno L. Alves, Nicholas D. Huntington, Antonio A. Freitas, Ana Cumano, Paulo Vieira

Research output: Contribution to journal › Article › Research › peer-review

15 Citations (Scopus)

Abstract

TLR9 is expressed in cells of the innate immune system, as well as in B lymphocytes and their progenitors. We investigated the effect of the TLR9 ligand CpG DNA on the proliferation of pro-B cells. CpG DNA inhibits the proliferation of pro-B, but not pre-B, cells by inducing caspase-independent cell death through a pathway that requires the expression of cathepsin B. This pathway is operative in Rag-deficient mice carrying an SP6 transgene, in which B lymphopoiesis is compromised, to reduce the size of the B lymphocyte precursor compartments in the bone marrow. Thus, TLR9 signals can regulate B lymphopoiesis in vivo.

Original language	English
Pages (from-to)	5678-5685
Number of pages	8
Journal	Journal of Immunology
Volume	184
Issue number	10
DOIs	https://doi.org/10.4049/jimmunol.0903854
Publication status	Published - 15 May 2010
Externally published	Yes

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title = "CpG inhibits pro-B cell expansion through a cathepsin B-dependent mechanism",

abstract = "TLR9 is expressed in cells of the innate immune system, as well as in B lymphocytes and their progenitors. We investigated the effect of the TLR9 ligand CpG DNA on the proliferation of pro-B cells. CpG DNA inhibits the proliferation of pro-B, but not pre-B, cells by inducing caspase-independent cell death through a pathway that requires the expression of cathepsin B. This pathway is operative in Rag-deficient mice carrying an SP6 transgene, in which B lymphopoiesis is compromised, to reduce the size of the B lymphocyte precursor compartments in the bone marrow. Thus, TLR9 signals can regulate B lymphopoiesis in vivo.",

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T1 - CpG inhibits pro-B cell expansion through a cathepsin B-dependent mechanism

AU - Lalanne, Ana Inés

AU - Moraga, Ignacio

AU - Hao, Yi

AU - Pereira, João Pedro

AU - Alves, Nuno L.

AU - Huntington, Nicholas D.

AU - Freitas, Antonio A.

AU - Cumano, Ana

AU - Vieira, Paulo

PY - 2010/5/15

Y1 - 2010/5/15

N2 - TLR9 is expressed in cells of the innate immune system, as well as in B lymphocytes and their progenitors. We investigated the effect of the TLR9 ligand CpG DNA on the proliferation of pro-B cells. CpG DNA inhibits the proliferation of pro-B, but not pre-B, cells by inducing caspase-independent cell death through a pathway that requires the expression of cathepsin B. This pathway is operative in Rag-deficient mice carrying an SP6 transgene, in which B lymphopoiesis is compromised, to reduce the size of the B lymphocyte precursor compartments in the bone marrow. Thus, TLR9 signals can regulate B lymphopoiesis in vivo.

AB - TLR9 is expressed in cells of the innate immune system, as well as in B lymphocytes and their progenitors. We investigated the effect of the TLR9 ligand CpG DNA on the proliferation of pro-B cells. CpG DNA inhibits the proliferation of pro-B, but not pre-B, cells by inducing caspase-independent cell death through a pathway that requires the expression of cathepsin B. This pathway is operative in Rag-deficient mice carrying an SP6 transgene, in which B lymphopoiesis is compromised, to reduce the size of the B lymphocyte precursor compartments in the bone marrow. Thus, TLR9 signals can regulate B lymphopoiesis in vivo.

UR - https://www.scopus.com/pages/publications/77954714801

U2 - 10.4049/jimmunol.0903854

DO - 10.4049/jimmunol.0903854

M3 - Article

C2 - 20400700

AN - SCOPUS:77954714801

SN - 0022-1767

VL - 184

SP - 5678

EP - 5685

JO - Journal of Immunology

JF - Journal of Immunology

IS - 10

ER -

CpG inhibits pro-B cell expansion through a cathepsin B-dependent mechanism

Abstract

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