The Experts below are selected from a list of 4263 Experts worldwide ranked by ideXlab platform
William Strober - One of the best experts on this subject based on the ideXlab platform.
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foxp3 regulatory t cells maintain the bone marrow microenvironment for b cell Lymphopoiesis
Nature Communications, 2017Co-Authors: Antonio Pierini, Hidekazu Nishikii, Jeanette Baker, Takaharu Kimura, Hyesook Kwon, Yuqiong Pan, Yan Chen, Maite Alvarez, William StroberAbstract:Foxp3+ regulatory T cells (Treg cells) modulate the immune system and maintain self-tolerance, but whether they affect haematopoiesis or haematopoietic stem cell (HSC)-mediated reconstitution after transplantation is unclear. Here we show that B-cell Lymphopoiesis is impaired in Treg-depleted mice, yet this reduced B-cell Lymphopoiesis is rescued by adoptive transfer of affected HSCs or bone marrow cells into Treg-competent recipients. B-cell reconstitution is abrogated in both syngeneic and allogeneic transplantation using Treg-depleted mice as recipients. Treg cells can control physiological IL-7 production that is indispensable for normal B-cell Lymphopoiesis and is mainly sustained by a subpopulation of ICAM1+ perivascular stromal cells. Our study demonstrates that Treg cells are important for B-cell differentiation from HSCs by maintaining immunological homoeostasis in the bone marrow microenvironment, both in physiological conditions and after bone marrow transplantation.
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foxp3 regulatory t cells maintain the bone marrow microenvironment for b cell Lymphopoiesis
Nature Communications, 2017Co-Authors: Antonio Pierini, Hidekazu Nishikii, Jeanette Baker, Takaharu Kimura, Hyesook Kwon, Yuqiong Pan, Yan Chen, Maite Alvarez, William StroberAbstract:Foxp3+ regulatory T cells (Treg cells) modulate the immune system and maintain self-tolerance, but whether they affect haematopoiesis or haematopoietic stem cell (HSC)-mediated reconstitution after transplantation is unclear. Here we show that B-cell Lymphopoiesis is impaired in Treg-depleted mice, yet this reduced B-cell Lymphopoiesis is rescued by adoptive transfer of affected HSCs or bone marrow cells into Treg-competent recipients. B-cell reconstitution is abrogated in both syngeneic and allogeneic transplantation using Treg-depleted mice as recipients. Treg cells can control physiological IL-7 production that is indispensable for normal B-cell Lymphopoiesis and is mainly sustained by a subpopulation of ICAM1+ perivascular stromal cells. Our study demonstrates that Treg cells are important for B-cell differentiation from HSCs by maintaining immunological homoeostasis in the bone marrow microenvironment, both in physiological conditions and after bone marrow transplantation. Treg cells suppress peripheral immune responses, but their function in haematopoiesis is unclear. Here the authors show they modulate the bone marrow microenvironment to sustain haematopoietic stem cell-driven generation of mature B cells.
Hidekazu Nishikii - One of the best experts on this subject based on the ideXlab platform.
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foxp3 regulatory t cells maintain the bone marrow microenvironment for b cell Lymphopoiesis
Nature Communications, 2017Co-Authors: Antonio Pierini, Hidekazu Nishikii, Jeanette Baker, Takaharu Kimura, Hyesook Kwon, Yuqiong Pan, Yan Chen, Maite Alvarez, William StroberAbstract:Foxp3+ regulatory T cells (Treg cells) modulate the immune system and maintain self-tolerance, but whether they affect haematopoiesis or haematopoietic stem cell (HSC)-mediated reconstitution after transplantation is unclear. Here we show that B-cell Lymphopoiesis is impaired in Treg-depleted mice, yet this reduced B-cell Lymphopoiesis is rescued by adoptive transfer of affected HSCs or bone marrow cells into Treg-competent recipients. B-cell reconstitution is abrogated in both syngeneic and allogeneic transplantation using Treg-depleted mice as recipients. Treg cells can control physiological IL-7 production that is indispensable for normal B-cell Lymphopoiesis and is mainly sustained by a subpopulation of ICAM1+ perivascular stromal cells. Our study demonstrates that Treg cells are important for B-cell differentiation from HSCs by maintaining immunological homoeostasis in the bone marrow microenvironment, both in physiological conditions and after bone marrow transplantation.
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foxp3 regulatory t cells maintain the bone marrow microenvironment for b cell Lymphopoiesis
Nature Communications, 2017Co-Authors: Antonio Pierini, Hidekazu Nishikii, Jeanette Baker, Takaharu Kimura, Hyesook Kwon, Yuqiong Pan, Yan Chen, Maite Alvarez, William StroberAbstract:Foxp3+ regulatory T cells (Treg cells) modulate the immune system and maintain self-tolerance, but whether they affect haematopoiesis or haematopoietic stem cell (HSC)-mediated reconstitution after transplantation is unclear. Here we show that B-cell Lymphopoiesis is impaired in Treg-depleted mice, yet this reduced B-cell Lymphopoiesis is rescued by adoptive transfer of affected HSCs or bone marrow cells into Treg-competent recipients. B-cell reconstitution is abrogated in both syngeneic and allogeneic transplantation using Treg-depleted mice as recipients. Treg cells can control physiological IL-7 production that is indispensable for normal B-cell Lymphopoiesis and is mainly sustained by a subpopulation of ICAM1+ perivascular stromal cells. Our study demonstrates that Treg cells are important for B-cell differentiation from HSCs by maintaining immunological homoeostasis in the bone marrow microenvironment, both in physiological conditions and after bone marrow transplantation. Treg cells suppress peripheral immune responses, but their function in haematopoiesis is unclear. Here the authors show they modulate the bone marrow microenvironment to sustain haematopoietic stem cell-driven generation of mature B cells.
Tatsuo Suda - One of the best experts on this subject based on the ideXlab platform.
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comparative effects of estrogen and raloxifene on b Lymphopoiesis and bone loss induced by sex steroid deficiency in mice
Journal of Bone and Mineral Research, 2010Co-Authors: Chisato Miyaura, Yoshiko Onoe, Masako Ito, Hiroaki Ohta, Shiro Nozawa, Tatsuo SudaAbstract:Estrogen deficiency caused by ovariectomy (OVX) results in a marked bone loss because of stimulated bone resorption. We have reported that OVX selectively stimulates B Lymphopoiesis in mouse bone marrow, which is somehow related to bone resorption. Estrogen prevents both the increased B Lymphopoiesis and the bone resorption caused by estrogen deficiency. Raloxifene also has a potent estrogenic activity for bone with minimal estrogenic activity for the uterus. To examine the effects of raloxifene on B Lymphopoiesis and bone resorption, OVX mice were given either estrogen or raloxifene subcutaneously for 2–4 weeks using a miniosmotic pump. Reduced uterine weight in OVX mice was restored completely by 17β-estradiol (E2). Some 300-fold higher doses of raloxifene increased uterine weight of OVX mice, but only slightly. The number of B220- positive pre-B cells was increased markedly in bone marrow after OVX. The increased B Lymphopoiesis was prevented not only by E2 but by raloxifene. In OVX mice, the trabecular bone volume (BV) of the femoral distal metaphysis was reduced markedly, when measured by microcomputed tomography (μCT) scanning and dual-energy X-ray absorptiometry. Both E2 and raloxifene similarly restored it. Like estrogen deficiency, androgen deficiency induced by orchidectomy (ORX) also resulted in a marked bone loss and increased B Lymphopoiesis. Both E2 and raloxifene prevented the changes in ORX mice. These results indicate that both estrogen deficiency and androgen deficiency similarly stimulate B Lymphopoiesis in mouse bone marrow, which accompany bone loss. Raloxifene exhibits estrogenic actions in bone and bone marrow to prevent bone loss and regulate B Lymphopoiesis without inducing estrogenic action in the uterus.
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increased b Lymphopoiesis by interleukin 7 induces bone loss in mice with intact ovarian function similarity to estrogen deficiency
Proceedings of the National Academy of Sciences of the United States of America, 1997Co-Authors: Chisato Miyaura, Yoshiko Onoe, Masaki Inada, Kazushige Maki, Koichi Ikuta, Masako Ito, Tatsuo SudaAbstract:Estrogen deficiency caused by ovariectomy (OVX) results in a marked bone loss due to stimulated bone resorption by osteoclasts. During our investigations of the pathogenesis of bone loss in estrogen deficiency, we found that OVX selectively stimulates B-Lymphopoiesis which results in marked accumulation of B220-positive pre-B cells in mouse bone marrow. To examine the possible correlation between stimulated B-Lymphopoiesis and bone loss, 8-week-old female mice were treated with interleukin (IL) 7, which stimulates B-Lymphopoiesis in bone marrow. We also examined bone mass in IL-7 receptor-knockout mice that exhibit marked suppression of B-Lymphopoiesis in the bone marrow. The increased B-Lymphopoiesis induced by IL-7 administration resulted in marked bone loss by stimulation of osteoclastic bone resorption in mice with intact ovarian function. The changes in both B-Lymphopoiesis and bone mass in IL-7-treated female mice were similar to those in age-matched OVX mice. In contrast, the trabecular bone volume of the femur was greatly increased in both female and male IL-7 receptor-knockout mice when compared with the respective wild-type and heterozygous littermates. These results show that the perturbation of B-Lymphopoiesis in the bone marrow is closely linked to the change in bone mass. We propose here that the increased B-Lymphopoiesis due to estrogen deficiency is involved in the mechanism of stimulated bone resorption.
Tomomitsu Hotta - One of the best experts on this subject based on the ideXlab platform.
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functional human t lymphocyte development from cord blood cd34 cells in nonobese diabetic shi scid il 2 receptor γ null mice
Journal of Immunology, 2002Co-Authors: Takashi Yahata, Kiyoshi Ando, Yoshihiko Nakamura, Yoshito Ueyama, Kazuo Shimamura, Norikazu Tamaoki, Shunichi Kato, Tomomitsu HottaAbstract:An experimental model for human T lymphocyte development from hemopoietic stem cells is necessary to study the complex processes of T cell differentiation in vivo. In this study, we report a newly developed nonobese diabetic (NOD)/Shi- scid , IL-2Rγ null (NOD/SCID/γc null ) mouse model for human T Lymphopoiesis. When these mice were transplanted with human cord blood CD34 + cells, the mice reproductively developed human T cells in their thymus and migrated into peripheral lymphoid organs. Furthermore, these T cells bear polyclonal TCR-αβ, and respond not only to mitogenic stimuli, such as PHA and IL-2, but to allogenic human cells. These results indicate that functional human T lymphocytes can be reconstituted from CD34 + cells in NOD/SCID/γc null mice. This newly developed mouse model is expected to become a useful tool for the analysis of human T Lymphopoiesis and immune response, and an animal model for studying T lymphotropic viral infections, such as HIV.
Warren S Pear - One of the best experts on this subject based on the ideXlab platform.
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notch signaling in Lymphopoiesis
Seminars in Immunology, 2003Co-Authors: Warren S Pear, Freddy RadtkeAbstract:Notch signaling regulates many cell fate decisions during development of multi-cellular organisms. Signals initiated by Notch influence a wide variety of processes that include lineage specification, cell survival and proliferation, and border formation. During development of the immune system, Notch has been shown to influence the fate of both hematopoietic stem cells (HSCs) and committed progenitors. Notch appears to play an especially important role in the development of cells that mediate acquired immunity where Notch influences multiple aspects of T and B cell development. In this review, we will focus on the potential functions of Notch signaling during lymphoid development.
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notch1 expression in early Lymphopoiesis influences b versus t lineage determination
Immunity, 1999Co-Authors: John C Pui, David Allman, Susan Derocco, Fredrick G Karnell, Sonia Bakkour, Julia Y Lee, Tom Kadesch, Richard R Hardy, Jon C Aster, Warren S PearAbstract:Notch receptors regulate fate decisions in many cells. One outcome of Notch signaling is differentiation of bipotential precursors into one cell type versus another. To investigate consequences of Notch1 expression in hematolymphoid progenitors, mice were reconstituted with bone marrow (BM) transduced with retroviruses encoding a constitutively active form of Notch1. Although neither granulocyte or monocyte differentiation were appreciably affected, Lymphopoiesis was dramatically altered. As early as 3 weeks following transplantation, mice receiving activated Notch1-transduced BM contained immature CD4+ CD8+ T cells in the BM and exhibited a simultaneous block in early B cell Lymphopoiesis. These results suggest that Notch1 provides a key regulatory signal in determining T lymphoid versus B lymphoid lineage decisions, possibly by influencing lineage commitment from a common lymphoid progenitor cell.
