Trim33/Tif1γ is involved in late stages of granulomonopoiesis in mice

Marie Lorraine Chrétien, Caroline Legouge, Romain Z. Martin, Arlette Hammann, Malika Trad, Romain Aucagne, Anne Largeot, Jean Noël Bastie, Laurent Delva*, Ronan Quéré

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

11 Citations (Scopus)

Abstract

Trim33/Tif1γ (Trim33) is a member of the tripartite motif family. Using a conditional hematopoietic-specific Trim33 knock-out (Trim33Δ/Δ) mouse, we showed previously that Trim33 deficiency in hematopoietic stem cells leads to severe defects in hematopoiesis, resembling the main features of human chronic myelomonocytic leukemia. We also demonstrated that Trim33 is involved in hematopoietic aging through TGFβ signaling. Nevertheless, how Trim33 contributes to the terminal stages of myeloid differentiation remains to be clarified. We reveal here the crucial role of Trim33 expression in the control of mature granulomonocytic differentiation. An important component of Trim33-deficient mice is the alteration of myeloid differentiation, as characterized by dysplastic features, abnormal granulocyte and monocyte maturation, and the expansion of CD11b+Ly6GhighLy6Clow myeloid cells, which share some features with polymorphonuclear-myeloid-derived suppressor cells. Moreover, in Trim33Δ/Δ mice, we observed the alteration of CSF-1-mediated macrophage differentiation in association with the lack of Csf-1 receptor. Altogether, these results indicate that Trim33 deficiency leads to the expansion of a subset of myeloid cells characterizing the myelodysplastic/myeloproliferative neoplasm.

Original languageEnglish
Pages (from-to)727-739.e6
JournalExperimental Hematology
Volume44
Issue number8
DOIs
Publication statusPublished - 1 Aug 2016
Externally publishedYes

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