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1-6 of 6
Rudi W. Hendriks
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Journal Articles
Maho Nagasawa, Balthasar A. Heesters, Chantal M.A. Kradolfer, Lisette Krabbendam, Itziar Martinez-Gonzalez, Marjolein J.W. de Bruijn, Korneliusz Golebski, Rudi W. Hendriks, Ralph Stadhouders, Hergen Spits, Suzanne M. Bal
Journal:
Journal of Experimental Medicine
Journal of Experimental Medicine (2019) 216 (9): 2221–2222.
Published: 06 August 2019
Journal Articles
KLRG1 and NKp46 discriminate subpopulations of human CD117 + CRTH2 − ILCs biased toward ILC2 or ILC3
Maho Nagasawa, Balthasar A. Heesters, Chantal M.A. Kradolfer, Lisette Krabbendam, Itziar Martinez-Gonzalez, Marjolein J.W. de Bruijn, Korneliusz Golebski, Rudi W. Hendriks, Ralph Stadhouders, Hergen Spits, Suzanne M. Bal
Journal:
Journal of Experimental Medicine
Journal of Experimental Medicine (2019) 216 (8): 1762–1776.
Published: 14 June 2019
Abstract
Recently, human ILCs that express CD117 and CD127 but lack CRTH2 and NKp44 have been shown to contain precursors of ILC1, ILC2, and ILC3. However, these ILCs have not been extensively characterized. We performed an unbiased hierarchical stochastic neighbor embedding (HSNE) analysis of the phenotype of peripheral blood CD117 + ILCs, which revealed the presence of three major subsets: the first expressed NKp46, the second expressed both NKp46 and CD56, and the third expressed KLRG1, but not NKp46 or CD56. Analysis of their cytokine production profiles and transcriptome revealed that NKp46 + ILCs predominantly develop into ILC3s; some of them can differentiate into ILC1/NK-like cells, but they are unable to develop into ILC2s. In contrast, KLRG1 + ILCs predominantly differentiate into ILC2s. Single-cell cultures demonstrate that KLRG1 + ILCs can also differentiate into other ILC subsets depending on the signals they receive. Epigenetic profiling of KLRG1 + ILCs is consistent with the broad differentiation potential of these cells.
Includes: Supplementary data
Journal Articles
Nicolas Serafini, Roel G.J. Klein Wolterink, Naoko Satoh-Takayama, Wei Xu, Christian A.J. Vosshenrich, Rudi W. Hendriks, James P. Di Santo
Journal:
Journal of Experimental Medicine
Journal of Experimental Medicine (2014) 211 (2): 199–208.
Published: 13 January 2014
Abstract
Group 3 innate lymphoid cells (ILC3) include IL-22–producing NKp46 + cells and IL-17A/IL-22–producing CD4 + lymphoid tissue inducerlike cells that express RORγt and are implicated in protective immunity at mucosal surfaces. Whereas the transcription factor Gata3 is essential for T cell and ILC2 development from hematopoietic stem cells (HSCs) and for IL-5 and IL-13 production by T cells and ILC2, the role for Gata3 in the generation or function of other ILC subsets is not known. We found that abundant GATA-3 protein is expressed in mucosa-associated ILC3 subsets with levels intermediate between mature B cells and ILC2. Chimeric mice generated with Gata3 -deficient fetal liver hematopoietic precursors lack all intestinal RORγt + ILC3 subsets, and these mice show defective production of IL-22 early after infection with the intestinal pathogen Citrobacter rodentium , leading to impaired survival. Further analyses demonstrated that ILC3 development requires cell-intrinsic Gata3 expression in fetal liver hematopoietic precursors. Our results demonstrate that Gata3 plays a generalized role in ILC lineage determination and is critical for the development of gut RORγt + ILC3 subsets that maintain mucosal barrier homeostasis. These results further extend the paradigm of Gata3 -dependent regulation of diversified innate ILC and adaptive T cell subsets.
Includes: Supplementary data
Journal Articles
Kam-Wing Ling, Katrin Ottersbach, Jan Piet van Hamburg, Aneta Oziemlak, Fong-Ying Tsai, Stuart H. Orkin, Rob Ploemacher, Rudi W. Hendriks, Elaine Dzierzak
Journal:
Journal of Experimental Medicine
Journal of Experimental Medicine (2004) 200 (7): 871–882.
Published: 04 October 2004
Abstract
GATA-2 is an essential transcription factor in the hematopoietic system that is expressed in hematopoietic stem cells (HSCs) and progenitors. Complete deficiency of GATA-2 in the mouse leads to severe anemia and embryonic lethality. The role of GATA-2 and dosage effects of this transcription factor in HSC development within the embryo and adult are largely unexplored. Here we examined the effects of GATA-2 gene dosage on the generation and expansion of HSCs in several hematopoietic sites throughout mouse development. We show that a haploid dose of GATA-2 severely reduces production and expansion of HSCs specifically in the aorta-gonad-mesonephros region (which autonomously generates the first HSCs), whereas quantitative reduction of HSCs is minimal or unchanged in yolk sac, fetal liver, and adult bone marrow. However, HSCs in all these ontogenically distinct anatomical sites are qualitatively defective in serial or competitive transplantation assays. Also, cytotoxic drug-induced regeneration studies show a clear GATA-2 dose–related proliferation defect in adult bone marrow. Thus, GATA-2 plays at least two functionally distinct roles during ontogeny of HSCs: the production and expansion of HSCs in the aorta-gonad-mesonephros and the proliferation of HSCs in the adult bone marrow.
Journal Articles
Uwe Schmidt, Emile van den Akker, Martine Parren-van Amelsvoort, Gabi Litos, Marella de Bruijn, Laura Gutiérrez, Rudi W. Hendriks, Wilfried Ellmeier, Bob Löwenberg, Hartmut Beug, Marieke von Lindern
Journal:
Journal of Experimental Medicine
Journal of Experimental Medicine (2004) 199 (7): 1033.
Published: 05 April 2004
Journal Articles
Uwe Schmidt, Emile van den Akker, Martine Parren-van Amelsvoort, Gabi Litos, Marella de Bruijn, Laura Gutiérrez, Rudi W. Hendriks, Wilfried Ellmeier, Bob Löwenberg, Hartmut Beug, Marieke von Lindern
Journal:
Journal of Experimental Medicine
Journal of Experimental Medicine (2004) 199 (6): 785–795.
Published: 08 March 2004
Abstract
Regulation of survival, expansion, and differentiation of erythroid progenitors requires the well-controlled activity of signaling pathways induced by erythropoietin (Epo) and stem cell factor (SCF). In addition to qualitative regulation of signaling pathways, quantitative control may be essential to control appropriate cell numbers in peripheral blood. We demonstrate that Bruton's tyrosine kinase (Btk) is able to associate with the Epo receptor (EpoR) and Jak2, and is a substrate of Jak2. Deficiency of Btk results in reduced and delayed phosphorylation of the EpoR, Jak2, and downstream signaling molecules such as Stat5 and PLCγ1 as well as in decreased responsiveness to Epo. As a result, expansion of erythroid progenitors lacking Btk is impaired at limiting concentrations of Epo and SCF. In addition, we show that SCF induces Btk to interact with TNF-related apoptosis-inducing ligand (TRAIL)–receptor 1 and that lack of Btk results in increased sensitivity to TRAIL-induced apoptosis. Together, our results indicate that Btk is a novel, quantitative regulator of Epo/SCF-dependent expansion and survival in erythropoiesis.
Includes: Supplementary data