Premature T cell senescence in Ovx mice is inhibited by repletion of estrogen and medicarpin: a possible mechanism for alleviating bone loss

Tyagi, Abdul Malik; Srivastava, Kirti; Kureel, Jyoti; Kumar, Amit; Raghuvanshi, Ashutosh; Yadav, Deepti; Maurya, Rakesh; Goel, Atul; Singh, Divya

doi:10.1007/s00198-011-1650-x

Cited by 48 publications

(53 citation statements)

References 44 publications

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“…In the mouse, this phenomenon results from enhanced thymic-dependent differentiation of BM-derived progenitors and IFNγ-driven peripheral expansion of mature T cells (57,64). Ovx also increases the population of premature senescent CD4 + CD28 -T cells (65), a lineage that produces high levels of TNF. Another factor responsible for the bone loss induced by estrogen deficiency is IL-17, the signature cytokine of Th17 cells (47), which are an osteoclastogenic subset of CD4 + T cells (45,46).…”

Section: Discussionmentioning

confidence: 99%

Sex steroid deficiency–associated bone loss is microbiota dependent and prevented by probiotics

Li¹,

Chassaing²,

Tyagi³

et al. 2016

Journal of Clinical Investigation

495

610

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Section: Discussionmentioning

confidence: 99%

Sex steroid deficiency–associated bone loss is microbiota dependent and prevented by probiotics

Li¹,

Chassaing²,

Tyagi³

et al. 2016

Journal of Clinical Investigation

495

610

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“…CD4 ϩ T cells, macrophages, and B cells were isolated using columns, Macs separator, and Micro beads from Miltenyi Biotech (Singapore) by positive selection. All the steps were performed using the manufacturer's instruction and as per as protocols in our previously published papers (10,24,35). After isolation the cells were collected in 1 ml of TRIzol (Invitrogen) for RNA isolation.…”

Section: Methodsmentioning

confidence: 99%

Interleukin 27 (IL-27) Alleviates Bone Loss in Estrogen-deficient Conditions by Induction of Early Growth Response-2 Gene

Shukla

Mansoori

Kakaji

et al. 2017

Journal of Biological Chemistry

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Edited by Xiao-Fan WangA growing understanding of the bone remodeling process suggests that inflammation significantly contributes to the pathogenesis of osteoporosis. T cells and various cytokines contribute majorly to the estrogen deficiency-induced bone loss. Recent studies have identified the IL-12 cytokine family as consisting of pro-inflammatory IL-12 and IL-23 and the anti-inflammatory IL-27 and IL-35 cytokines. IL-27 exerts protective effects in autoimmune diseases like experimental autoimmune encephalomyelitis; however, its role in the pathogenesis of osteoporosis remains to be determined. In this report, we study the effect of IL-27 supplementation on ovariectomized estrogen-deficient mice on various immune and skeletal parameters. IL-27 treatment in ovariectomized mice suppressed Th17 cell differentiation by inhibiting transcription factor ROR␥t. Supplementation of IL-27 activates Egr-2 to induce IL-10 producing Tr1 cells. IL-27 treatment prevented the loss of trabecular micro-architecture and preservedcorticalboneparameters.IL-27alsoinhibitedosteoblastapo-ptosis through increased Egr-2 expression, which induces antiapoptotic factors like MCL-1. IL-27 suppressed osteoclastogenesis in an Egr-2-dependent manner that up-regulates Id2, the repressor of the receptor activator of nuclear factor-B ligand-mediated osteoclastogenesis. Additionally, these results were corroborated in female osteoporotic subjects where we found decreased serum IL-27 levels along with reduced Egr-2 expression. Our study forms a strong basis for using humanized IL-27 toward the treatment of post-menopausal osteoporosis.

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“…In response to ovx, ROS are produced by most BM cells including T cells (52). ROS play an important role in postmenopausal bone loss by generating a more oxidized bone microenvironment (53,54).…”

Section: T Cells Mediate the Effects Of Estrogen Deficiency In Bonementioning

confidence: 99%

Osteoimmunology and Its Implications for Transplantation

Pacifici

2013

American Journal of Transplantation

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Osteoimmunology is a field of research dedicated to the study of the interactions between the immune system, the hemopoietic system and bone. Among the cells of the immune system that regulate bone cells and the hemopoietic function are T lymphocytes. These cells secrete inflammatory cytokines that promote bone resorption, as well as Wnt ligands that stimulate bone formation. In addition, T cells regulate bone homeostasis by cross talking with BM stromal cells and osteoblastic cells via CD40 ligand (CD40L) and other costimulatory molecules. This article describes the immune cells relevant to bone and the hemopoietic function, reviews the role of lymphocytes as mediators of the effects of PTH and estrogen in bone and the hemopoietic system and discusses the implication of osteoimmunology for transplant medicine.

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Premature T cell senescence in Ovx mice is inhibited by repletion of estrogen and medicarpin: a possible mechanism for alleviating bone loss

Cited by 48 publications

References 44 publications

Sex steroid deficiency–associated bone loss is microbiota dependent and prevented by probiotics

Sex steroid deficiency–associated bone loss is microbiota dependent and prevented by probiotics

Interleukin 27 (IL-27) Alleviates Bone Loss in Estrogen-deficient Conditions by Induction of Early Growth Response-2 Gene

Osteoimmunology and Its Implications for Transplantation

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