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Article ; Online: Decreased production of class-switched antibodies in neonatal B cells is associated with increased expression of miR-181b.

Glaesener, Stephanie / Jaenke, Christine / Habener, Anika / Geffers, Robert / Hagendorff, Petra / Witzlau, Katrin / Imelmann, Esther / Krueger, Andreas / Meyer-Bahlburg, Almut

PloS one

2018 Volume 13, Issue 2, Page(s) e0192230

Abstract: The increased susceptibility to infections of neonates is caused by an immaturity of the immune system as a result of both qualitative and quantitative differences between neonatal and adult immune cells. With respect to B cells, neonatal antibody ... ...

Abstract	The increased susceptibility to infections of neonates is caused by an immaturity of the immune system as a result of both qualitative and quantitative differences between neonatal and adult immune cells. With respect to B cells, neonatal antibody responses are known to be decreased. Accountable for this is an altered composition of the neonatal B cell compartment towards more immature B cells. However, it remains unclear whether the functionality of individual neonatal B cell subsets is altered as well. In the current study we therefore compared phenotypical and functional characteristics of corresponding neonatal and adult B cell subpopulations. No phenotypic differences could be identified with the exception of higher IgM expression in neonatal B cells. Functional analysis revealed differences in proliferation, survival, and B cell receptor signaling. Most importantly, neonatal B cells showed severely impaired class-switch recombination (CSR) to IgG and IgA. This was associated with increased expression of miR-181b in neonatal B cells. Deficiency of miR-181b resulted in increased CSR. With this, our results highlight intrinsic differences that contribute to weaker B cell antibody responses in newborns.
MeSH term(s)	Animals ; B-Lymphocytes/immunology ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Humans ; Immunoglobulin Class Switching/immunology ; Infant, Newborn ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics
Chemical Substances	MIRN-181 microRNA, human ; MicroRNAs
Language	English
Publishing date	2018
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0192230
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Chemokine receptor CX3CR1 promotes dendritic cell development under steady-state conditions.

Łyszkiewicz, Marcin / Witzlau, Katrin / Pommerencke, Jens / Krueger, Andreas

European journal of immunology

2011 Volume 41, Issue 5, Page(s) 1256–1265

Abstract: Expression of CX3CR1 is an attribute of myeloid precursors committed to the monocyte/macrophage (Mφ)/DC lineages and is maintained during all stages of DC differentiation. Nevertheless, the exact role of this molecule during developmental progression of ... ...

Abstract	Expression of CX3CR1 is an attribute of myeloid precursors committed to the monocyte/macrophage (Mφ)/DC lineages and is maintained during all stages of DC differentiation. Nevertheless, the exact role of this molecule during developmental progression of myeloid precursors towards the DC lineage remains elusive. To overcome potential compensatory mechanisms and issues of redundancy, we employed competitive adoptive transfer experiments to assess a possible function of CX3CR1 in DC and monocyte/Mφ differentiation in vivo. We show here that expression of CX3CR1 promotes the generation of DCs and monocytes/Mφ under steady-state conditions and during compensatory expansion after selective depletion of DCs, but not under inflammatory conditions evoked by sub-lethal irradiation. Direct administration of CX3CR1-deficient and CX3CR1-sufficient precursors into the spleen or the thymus resulted in a similar competitive advantage of WT over CX3CR1-deficient precursors as i.v. transfer, suggesting that CX3CR1-mediated survival rather than recruitment to lymphoid organs is critical for DC/Mφ differentiation. In conclusion, our data support the hypothesis that CX3CR1 promotes proper development of myeloid precursors into DCs and monocytes/Mφs under steady-state conditions, possibly by providing survival signals or mediating accessibility to organ-specific niches, rather than acting as a mediator of homing to the spleen or the thymus.
MeSH term(s)	Adoptive Transfer ; Animals ; Antibodies, Monoclonal ; CX3C Chemokine Receptor 1 ; Cell Differentiation ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Dendritic Cells/physiology ; Dendritic Cells/radiation effects ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Inflammation/immunology ; Macrophages/immunology ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Monocyte-Macrophage Precursor Cells/metabolism ; Monocytes/immunology ; Monocytes/metabolism ; Receptors, Chemokine/genetics ; Receptors, Chemokine/metabolism ; Receptors, Chemokine/radiation effects ; Signal Transduction
Chemical Substances	Antibodies, Monoclonal ; CX3C Chemokine Receptor 1 ; Cx3cr1 protein, mouse ; Receptors, Chemokine
Language	English
Publishing date	2011-05
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201040977
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Article ; Online: MicroRNA-181a/b-1 Is Not Required for Innate γδ NKT Effector Cell Development.

Sandrock, Inga / Ziętara, Natalia / Łyszkiewicz, Marcin / Oberdörfer, Linda / Witzlau, Katrin / Krueger, Andreas / Prinz, Immo

PloS one

2015 Volume 10, Issue 12, Page(s) e0145010

Abstract: Thymic development of αβ T lymphocytes into invariant natural killer (NK) T cells depends on their selection via agonistic lipid antigen presented by CD1d. If successful, newly selected NKT cells gain effector functions already in the thymus. Some γδ T ... ...

Abstract	Thymic development of αβ T lymphocytes into invariant natural killer (NK) T cells depends on their selection via agonistic lipid antigen presented by CD1d. If successful, newly selected NKT cells gain effector functions already in the thymus. Some γδ T cell subsets also acquire effector functions in the thymus. However, it is not clear whether agonistic TCR stimulation is involved in thymic γδ T cell selection and development. Here we combine two genetic models to address this question. MiR-181a/b-1-/-mice, which show impaired agonistic T cell selection of invariant αβ NKT cells, were crossed to Tcrd-H2BeGFP reporter mice to monitor selection, intra-thymic expansion and differentiation of γδ T cells. We found that miR-181a/b-1-deficiency had no effect on numbers of thymic γδ T cell or on their differentiation towards an IL-17- or IFN-γ-producing effector phenotype. Also, the composition of peripheral lymph node γδ T cells was not affected by miR-181a/b-1-deficiency. Dendritic epidermal γδ T cells were normally present in knock-out animals. However, we observed elevated frequencies and numbers of γδ NKT cells in the liver, possibly because γδ NKT cells can expand and replace missing αβ NKT cells in peripheral niches. In summary, we investigated the role of miR-181a/b-1 for selection, intrathymic development and homeostasis of γδ T cells. We conclude that miR-181a/b-1-dependent modulation of T cell selection is not critically required for innate development of γδ NKT cells or of any other γδ T cell subtypes.
MeSH term(s)	Animals ; Antigens, CD1d/metabolism ; Cell Differentiation/genetics ; Clonal Selection, Antigen-Mediated/genetics ; Immunity, Innate ; Immunophenotyping ; Liver/cytology ; Liver/immunology ; Lymph Nodes/cytology ; Lymph Nodes/immunology ; Lymph Nodes/metabolism ; Mice ; Mice, Knockout ; Mice, Transgenic ; MicroRNAs/genetics ; Natural Killer T-Cells/cytology ; Natural Killer T-Cells/immunology ; Natural Killer T-Cells/metabolism ; Phenotype ; Receptors, Antigen, T-Cell, gamma-delta/metabolism ; T-Cell Antigen Receptor Specificity/immunology ; T-Lymphocyte Subsets/cytology ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; Thymus Gland/cytology ; Thymus Gland/immunology ; Thymus Gland/metabolism
Chemical Substances	Antigens, CD1d ; MicroRNAs ; Receptors, Antigen, T-Cell, gamma-delta ; mirn181 microRNA, mouse
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0145010
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Article ; Online: Extra-thymic physiological T lineage progenitor activity is exclusively confined to cells expressing either CD127, CD90, or high levels of CD117.

Saran, Namita / Pommerencke, Jens / Witzlau, Katrin / Regelin, Malte / Krueger, Andreas

PloS one

2012 Volume 7, Issue 2, Page(s) e30864

Abstract: T cell development depends on continuous recruitment of progenitors from bone marrow (BM) to the thymus via peripheral blood. However, both phenotype and functional characteristics of physiological T cell precursors remain ill-defined. Here, we ... ...

Abstract	T cell development depends on continuous recruitment of progenitors from bone marrow (BM) to the thymus via peripheral blood. However, both phenotype and functional characteristics of physiological T cell precursors remain ill-defined. Here, we characterized a putative CD135(+)CD27(+) T cell progenitor population, which lacked expression of CD127, CD90, and high levels of CD117 and was therefore termed triple negative precursor (TNP). TNPs were present in both BM and blood and displayed robust T lineage potential, but virtually no myeloid or B lineage potential, in vitro. However, TNPs did not efficiently generate T lineage progeny after intravenous or intrathymic transfer, suggesting that a physiological thymic microenvironment does not optimally support T cell differentiation from TNPs. Thus, we propose that physiological T cell precursors are confined to populations expressing either CD127, CD90, or high levels of CD117 in addition to CD135 and CD27 and that TNPs may have other physiological functions.
MeSH term(s)	Animals ; Bone Marrow/immunology ; Bone Marrow/metabolism ; Cell Differentiation ; Cell Lineage ; Cells, Cultured ; Flow Cytometry ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/immunology ; Hematopoietic Stem Cells/metabolism ; Interleukin-7 Receptor alpha Subunit/metabolism ; Leukocyte Common Antigens/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Proto-Oncogene Proteins c-kit/metabolism ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Thy-1 Antigens/metabolism ; Thymus Gland/cytology ; Thymus Gland/immunology ; Thymus Gland/metabolism
Chemical Substances	Interleukin-7 Receptor alpha Subunit ; Thy-1 Antigens ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1) ; Leukocyte Common Antigens (EC 3.1.3.48)
Language	English
Publishing date	2012-02-15
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0030864
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Article ; Online: Overexpression of Vα14Jα18 TCR promotes development of iNKT cells in the absence of miR-181a/b-1.

Blume, Jonas / Zur Lage, Susanne / Witzlau, Katrin / Georgiev, Hristo / Weiss, Siegfried / Łyszkiewicz, Marcin / Ziȩtara, Natalia / Krueger, Andreas

Immunology and cell biology

2016 Volume 94, Issue 8, Page(s) 741–746

Abstract: Expression of microRNA miR-181a/b-1 is critical for intrathymic development of invariant natural killer T (iNKT) cells. However, the underlying mechanism has remained a matter of debate. On the one hand, growing evidence suggested that miR-181a/b-1 is ... ...

Abstract	Expression of microRNA miR-181a/b-1 is critical for intrathymic development of invariant natural killer T (iNKT) cells. However, the underlying mechanism has remained a matter of debate. On the one hand, growing evidence suggested that miR-181a/b-1 is instrumental in setting T-cell receptor (TCR) signaling threshold and thus permits agonist selection of iNKT cells through high-affinity TCR ligands. On the other hand, alterations in metabolic fitness mediated by miR-181a/b-1-dependent dysregulation of phosphatase and tensin homolog (Pten) have been proposed to cause the iNKT-cell defect in miR-181-a/b-1-deficient mice. To re-assess the hypothesis that modulation of TCR signal strength is the key mechanism by which miR-181a/b-1 controls the development of iNKT cells, we generated miR-181a/b-1-deficient mice expressing elevated levels of a Vα14Jα18 TCRα chain. In these mice, development of iNKT cells was fully restored. Furthermore, both subset distribution of iNKT cells as well as TCR Vβ repertoire were independent of the presence of miR-181a/b-1 once a Vα14Jα18 TCRα chain was overexpressed. Finally, levels of Pten protein were similar in Vα14Jα18 transgenic mice irrespective of their miR-181a/b-1 status. Collectively, our data support a model in which miR-181 promotes development of iNKT cells primarily by generating a permissive state for agonist selection with alterations in metabolic fitness possibly constituting a secondary effect.
MeSH term(s)	Animals ; Cell Polarity ; Lymphocyte Subsets/immunology ; Mice, Transgenic ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Natural Killer T-Cells/cytology ; Natural Killer T-Cells/metabolism ; PTEN Phosphohydrolase/metabolism ; Receptors, Antigen, T-Cell, alpha-beta/metabolism ; Transgenes
Chemical Substances	MicroRNAs ; Receptors, Antigen, T-Cell, alpha-beta ; mirn181 microRNA, mouse ; PTEN Phosphohydrolase (EC 3.1.3.67)
Language	English
Publishing date	2016-05-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	284057-1
ISSN	1440-1711 ; 0818-9641
ISSN (online)	1440-1711
ISSN	0818-9641
DOI	10.1038/icb.2016.40
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Article ; Online: Responsiveness of Developing T Cells to IL-7 Signals Is Sustained by miR-17∼92.

Regelin, Malte / Blume, Jonas / Pommerencke, Jens / Vakilzadeh, Ramin / Witzlau, Katrin / Łyszkiewicz, Marcin / Ziętara, Natalia / Saran, Namita / Schambach, Axel / Krueger, Andreas

Journal of immunology (Baltimore, Md. : 1950)

2015 Volume 195, Issue 10, Page(s) 4832–4840

Abstract: miRNAs regulate a large variety of developmental processes including development of the immune system. T cell development is tightly controlled through the interplay of transcriptional programs and cytokine-mediated signals. However, the role of ... ...

Abstract	miRNAs regulate a large variety of developmental processes including development of the immune system. T cell development is tightly controlled through the interplay of transcriptional programs and cytokine-mediated signals. However, the role of individual miRNAs in this process remains largely elusive. In this study, we demonstrated that hematopoietic cell-specific loss of miR-17∼92, a cluster of six miRNAs implicated in B and T lineage leukemogenesis, resulted in profound defects in T cell development both at the level of prethymic T cell progenitors as well as intrathymically. We identified reduced surface expression of IL-7R and concomitant limited responsiveness to IL-7 signals as a common mechanism resulting in reduced cell survival of common lymphoid progenitors and thymocytes at the double-negative to double-positive transition. In conclusion, we identified miR-17∼92 as a critical modulator of multiple stages of T cell development.
MeSH term(s)	Animals ; Animals, Genetically Modified ; B-Lymphocytes/cytology ; B-Lymphocytes/immunology ; Cell Survival/genetics ; Cell Survival/immunology ; Interleukin-7/genetics ; Interleukin-7/immunology ; Mice ; MicroRNAs/genetics ; MicroRNAs/immunology ; Receptors, Interleukin-17/genetics ; Receptors, Interleukin-17/immunology ; Signal Transduction/physiology ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology
Chemical Substances	Il17r protein, mouse ; Interleukin-7 ; MicroRNAs ; Mirn17 microRNA, mouse ; Receptors, Interleukin-17 ; interleukin-7, mouse
Language	English
Publishing date	2015-11-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1402248
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Article ; Online: Multicongenic fate mapping quantification of dynamics of thymus colonization.

Ziętara, Natalia / Łyszkiewicz, Marcin / Puchałka, Jacek / Witzlau, Katrin / Reinhardt, Annika / Förster, Reinhold / Pabst, Oliver / Prinz, Immo / Krueger, Andreas

The Journal of experimental medicine

2015 Volume 212, Issue 10, Page(s) 1589–1601

Abstract: Postnatal T cell development depends on continuous colonization of the thymus by BM-derived T lineage progenitors. Both quantitative parameters and the mechanisms of thymus seeding remain poorly understood. Here, we determined the number of dedicated ... ...

Abstract	Postnatal T cell development depends on continuous colonization of the thymus by BM-derived T lineage progenitors. Both quantitative parameters and the mechanisms of thymus seeding remain poorly understood. Here, we determined the number of dedicated thymus-seeding progenitor niches (TSPNs) capable of supporting productive T cell development, turnover rates of niche occupancy, and feedback mechanisms. To this end, we established multicongenic fate mapping combined with mathematical modeling to quantitate individual events of thymus colonization. We applied this method to study thymus colonization in CCR7(-/-)CCR9(-/-) (DKO) mice, whose TSPNs are largely unoccupied. We showed that ∼160-200 TSPNs are present in the adult thymus and, on average, 10 of these TSPNs were open for recolonization at steady state. Preconditioning of wild-type mice revealed a similar number of TSPNs, indicating that preconditioning can generate space efficiently for transplanted T cell progenitors. To identify potential cellular feedback loops restricting thymus colonization, we performed serial transfer experiments. These experiments indicated that thymus seeding was directly restricted by the duration of niche occupancy rather than long-range effects, thus challenging current paradigms of thymus colonization.
MeSH term(s)	Animals ; Cell Lineage ; Mice, Inbred C57BL ; Mice, Knockout ; Receptors, CCR/genetics ; Receptors, CCR/metabolism ; Receptors, CCR7/genetics ; Receptors, CCR7/metabolism ; Receptors, Interleukin-17/genetics ; Stem Cells/physiology ; T-Lymphocytes/cytology ; T-Lymphocytes/physiology ; Thymocytes/physiology ; Thymus Gland/cytology ; Thymus Gland/physiology ; Thymus Gland/radiation effects
Chemical Substances	CC chemokine receptor 9 ; Ccr7 protein, mouse ; Il17r protein, mouse ; Receptors, CCR ; Receptors, CCR7 ; Receptors, Interleukin-17
Language	English
Publishing date	2015-09-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20142143
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Article ; Online: Decreased production of class-switched antibodies in neonatal B cells is associated with increased expression of miR-181b.

Glaesener, Stephanie / Jaenke, Christine / Habener, Anika / Geffers, Robert / Hagendorff, Petra / Witzlau, Katrin / Imelmann, Esther / Krueger, Andreas / Meyer-Bahlburg, Almut

2018

Abstract	The increased susceptibility to infections of neonates is caused by an immaturity of the immune system as a result of both qualitative and quantitative differences between neonatal and adult immune cells. With respect to B cells, neonatal antibody responses are known to be decreased. Accountable for this is an altered composition of the neonatal B cell compartment towards more immature B cells. However, it remains unclear whether the functionality of individual neonatal B cell subsets is altered as well. In the current study we therefore compared phenotypical and functional characteristics of corresponding neonatal and adult B cell subpopulations. No phenotypic differences could be identified with the exception of higher IgM expression in neonatal B cells. Functional analysis revealed differences in proliferation, survival, and B cell receptor signaling. Most importantly, neonatal B cells showed severely impaired class-switch recombination (CSR) to IgG and IgA. This was associated with increased expression of miR-181b in neonatal B cells. Deficiency of miR-181b resulted in increased CSR. With this, our results highlight intrinsic differences that contribute to weaker B cell antibody responses in newborns.
Language	English
Publishing country	de
Document type	Article ; Online
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Article ; Online: Decreased production of class-switched antibodies in neonatal B cells is associated with increased expression of miR-181b.

Glaesener, Stephanie / Jaenke, Christine / Habener, Anika / Geffers, Robert / Hagendorff, Petra / Witzlau, Katrin / Imelmann, Esther / Krueger, Andreas / Meyer-Bahlburg, Almut

2018

Abstract	The increased susceptibility to infections of neonates is caused by an immaturity of the immune system as a result of both qualitative and quantitative differences between neonatal and adult immune cells. With respect to B cells, neonatal antibody responses are known to be decreased. Accountable for this is an altered composition of the neonatal B cell compartment towards more immature B cells. However, it remains unclear whether the functionality of individual neonatal B cell subsets is altered as well. In the current study we therefore compared phenotypical and functional characteristics of corresponding neonatal and adult B cell subpopulations. No phenotypic differences could be identified with the exception of higher IgM expression in neonatal B cells. Functional analysis revealed differences in proliferation, survival, and B cell receptor signaling. Most importantly, neonatal B cells showed severely impaired class-switch recombination (CSR) to IgG and IgA. This was associated with increased expression of miR-181b in neonatal B cells. Deficiency of miR-181b resulted in increased CSR. With this, our results highlight intrinsic differences that contribute to weaker B cell antibody responses in newborns.
Language	English
Publishing country	de
Document type	Article ; Online
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Article ; Online: Limited niche availability suppresses murine intrathymic dendritic-cell development from noncommitted progenitors.

Łyszkiewicz, Marcin / Ziętara, Natalia / Föhse, Lisa / Puchałka, Jacek / Diestelhorst, Jana / Witzlau, Katrin / Prinz, Immo / Schambach, Axel / Krueger, Andreas

Blood

2014 Volume 125, Issue 3, Page(s) 457–464

Abstract: The origins of dendritic cells (DCs) and other myeloid cells in the thymus have remained controversial. In this study, we assessed developmental relationships between thymic dendritic cells and thymocytes, employing retrovirus-based cellular barcoding ... ...

Abstract	The origins of dendritic cells (DCs) and other myeloid cells in the thymus have remained controversial. In this study, we assessed developmental relationships between thymic dendritic cells and thymocytes, employing retrovirus-based cellular barcoding and reporter mice, as well as intrathymic transfers coupled with DC depletion. We demonstrated that a subset of early T-lineage progenitors expressed CX3CR1, a bona fide marker for DC progenitors. However, intrathymic transfers into nonmanipulated mice, as well as retroviral barcoding, indicated that thymic dendritic cells and thymocytes were largely of distinct developmental origin. In contrast, intrathymic transfers after in vivo depletion of DCs resulted in intrathymic development of non-T-lineage cells. In conclusion, our data support a model in which the adoption of T-lineage fate by noncommitted progenitors at steady state is enforced by signals from the thymic microenvironment unless niches promoting alternative lineage fates become available.
MeSH term(s)	Animals ; Cell Differentiation ; Cell Lineage ; Cells, Cultured ; Dendritic Cells/cytology ; Dendritic Cells/immunology ; Flow Cytometry ; Mice ; Mice, Inbred C57BL ; Myeloid Cells/cytology ; Myeloid Cells/immunology ; Stem Cell Niche/immunology ; Stem Cells/cytology ; Stem Cells/immunology ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology ; Thymus Gland/cytology ; Thymus Gland/immunology
Language	English
Publishing date	2014-11-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2014-07-592667
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