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CD4+ 1 T cells alter the stromal microenvironment and repress medullary erythropoiesis in murine visceral leishmaniasis.

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CD4+ 1 T cells alter the stromal microenvironment and repress medullary erythropoiesis in murine visceral leishmaniasis. / Preham, Olivier Yvon Giuseppe; Pinho, Flaviane Alves; Pinto, Ana Isabel; Rani, Gulab Fatima; Brown, Najmeeyah; Hitchcock, Ian Stuart; Goto, Hiro; Kaye, Paul.

In: Frontiers in immunology, Vol. 9, 2958, 18.12.2018.

Research output: Contribution to journalArticlepeer-review

Harvard

Preham, OYG, Pinho, FA, Pinto, AI, Rani, GF, Brown, N, Hitchcock, IS, Goto, H & Kaye, P 2018, 'CD4+ 1 T cells alter the stromal microenvironment and repress medullary erythropoiesis in murine visceral leishmaniasis.', Frontiers in immunology, vol. 9, 2958. https://doi.org/10.3389/fimmu.2018.02958

APA

Preham, O. Y. G., Pinho, F. A., Pinto, A. I., Rani, G. F., Brown, N., Hitchcock, I. S., Goto, H., & Kaye, P. (2018). CD4+ 1 T cells alter the stromal microenvironment and repress medullary erythropoiesis in murine visceral leishmaniasis. Frontiers in immunology, 9, [2958]. https://doi.org/10.3389/fimmu.2018.02958

Vancouver

Preham OYG, Pinho FA, Pinto AI, Rani GF, Brown N, Hitchcock IS et al. CD4+ 1 T cells alter the stromal microenvironment and repress medullary erythropoiesis in murine visceral leishmaniasis. Frontiers in immunology. 2018 Dec 18;9. 2958. https://doi.org/10.3389/fimmu.2018.02958

Author

Preham, Olivier Yvon Giuseppe ; Pinho, Flaviane Alves ; Pinto, Ana Isabel ; Rani, Gulab Fatima ; Brown, Najmeeyah ; Hitchcock, Ian Stuart ; Goto, Hiro ; Kaye, Paul. / CD4+ 1 T cells alter the stromal microenvironment and repress medullary erythropoiesis in murine visceral leishmaniasis. In: Frontiers in immunology. 2018 ; Vol. 9.

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@article{8a3611d9fc5f4423a0804b65ece56343,
title = "CD4+ 1 T cells alter the stromal microenvironment and repress medullary erythropoiesis in murine visceral leishmaniasis.",
abstract = "Human visceral leishmaniasis, a parasitic disease of major public health importance in developing countries, is characterized by variable degrees of severity of anemia, but the mechanisms underlying this change in peripheral blood have not been thoroughly explored. Here, we used an experimental model of visceral leishmaniasis in C57BL/6 mice to explore the basis of anemia following infection with Leishmania donovani. 28 days post infection,mice showed bone marrow dyserythropoiesis by myelogram, with a reduction of TER119+ CD71-/+ erythroblasts. Reduction of medullary erythropoiesis coincided with loss of CD169high bone marrow stromal macrophages and a reduction of CXCL12-expressing stromal cells. Although the spleen is a site of extramedullary erythropoiesis and erythrophagocytosis, splenectomy did not impact the extent of anemia or affect the repression of medullary hematopoiesis that was observed in infected mice. In contrast, these changes in bone marrow erythropoiesis were not evident in B6.Rag2 -/- mice, but could be fully reconstituted by adoptive transfer of IFNg-producing but not IFNg-deficient CD4+ T cells, mimicking the expansion of IFNg-producing CD4+ T cells that occurs during infection in wild type mice. Collectively, these data indicate that anemia during experimental murine visceral leishmaniasis can be driven by defects associated with the bone marrow erythropoietic niche, and that this represents a further example of CD4+ T cell-mediated immunopathology affecting hematopoietic competence.",
keywords = "bone marrow, erythropoiesis, leishmaniasis, macrophages, stromal cells",
author = "Preham, {Olivier Yvon Giuseppe} and Pinho, {Flaviane Alves} and Pinto, {Ana Isabel} and Rani, {Gulab Fatima} and Najmeeyah Brown and Hitchcock, {Ian Stuart} and Hiro Goto and Paul Kaye",
note = "{\textcopyright} 2018 Preham, Alves de Pinho, Pinto, Rani, Brown, Hitchcock, Goto and Kaye. ",
year = "2018",
month = dec,
day = "18",
doi = "10.3389/fimmu.2018.02958",
language = "English",
volume = "9",
journal = "Frontiers in immunology",
issn = "1664-3224",
publisher = "Frontiers Media S.A.",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - CD4+ 1 T cells alter the stromal microenvironment and repress medullary erythropoiesis in murine visceral leishmaniasis.

AU - Preham, Olivier Yvon Giuseppe

AU - Pinho, Flaviane Alves

AU - Pinto, Ana Isabel

AU - Rani, Gulab Fatima

AU - Brown, Najmeeyah

AU - Hitchcock, Ian Stuart

AU - Goto, Hiro

AU - Kaye, Paul

N1 - © 2018 Preham, Alves de Pinho, Pinto, Rani, Brown, Hitchcock, Goto and Kaye.

PY - 2018/12/18

Y1 - 2018/12/18

N2 - Human visceral leishmaniasis, a parasitic disease of major public health importance in developing countries, is characterized by variable degrees of severity of anemia, but the mechanisms underlying this change in peripheral blood have not been thoroughly explored. Here, we used an experimental model of visceral leishmaniasis in C57BL/6 mice to explore the basis of anemia following infection with Leishmania donovani. 28 days post infection,mice showed bone marrow dyserythropoiesis by myelogram, with a reduction of TER119+ CD71-/+ erythroblasts. Reduction of medullary erythropoiesis coincided with loss of CD169high bone marrow stromal macrophages and a reduction of CXCL12-expressing stromal cells. Although the spleen is a site of extramedullary erythropoiesis and erythrophagocytosis, splenectomy did not impact the extent of anemia or affect the repression of medullary hematopoiesis that was observed in infected mice. In contrast, these changes in bone marrow erythropoiesis were not evident in B6.Rag2 -/- mice, but could be fully reconstituted by adoptive transfer of IFNg-producing but not IFNg-deficient CD4+ T cells, mimicking the expansion of IFNg-producing CD4+ T cells that occurs during infection in wild type mice. Collectively, these data indicate that anemia during experimental murine visceral leishmaniasis can be driven by defects associated with the bone marrow erythropoietic niche, and that this represents a further example of CD4+ T cell-mediated immunopathology affecting hematopoietic competence.

AB - Human visceral leishmaniasis, a parasitic disease of major public health importance in developing countries, is characterized by variable degrees of severity of anemia, but the mechanisms underlying this change in peripheral blood have not been thoroughly explored. Here, we used an experimental model of visceral leishmaniasis in C57BL/6 mice to explore the basis of anemia following infection with Leishmania donovani. 28 days post infection,mice showed bone marrow dyserythropoiesis by myelogram, with a reduction of TER119+ CD71-/+ erythroblasts. Reduction of medullary erythropoiesis coincided with loss of CD169high bone marrow stromal macrophages and a reduction of CXCL12-expressing stromal cells. Although the spleen is a site of extramedullary erythropoiesis and erythrophagocytosis, splenectomy did not impact the extent of anemia or affect the repression of medullary hematopoiesis that was observed in infected mice. In contrast, these changes in bone marrow erythropoiesis were not evident in B6.Rag2 -/- mice, but could be fully reconstituted by adoptive transfer of IFNg-producing but not IFNg-deficient CD4+ T cells, mimicking the expansion of IFNg-producing CD4+ T cells that occurs during infection in wild type mice. Collectively, these data indicate that anemia during experimental murine visceral leishmaniasis can be driven by defects associated with the bone marrow erythropoietic niche, and that this represents a further example of CD4+ T cell-mediated immunopathology affecting hematopoietic competence.

KW - bone marrow

KW - erythropoiesis

KW - leishmaniasis

KW - macrophages

KW - stromal cells

UR - http://www.scopus.com/inward/record.url?scp=85059928178&partnerID=8YFLogxK

U2 - 10.3389/fimmu.2018.02958

DO - 10.3389/fimmu.2018.02958

M3 - Article

C2 - 30619317

VL - 9

JO - Frontiers in immunology

JF - Frontiers in immunology

SN - 1664-3224

M1 - 2958

ER -