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Article ; Online: Histone butyrylation in the mouse intestine is mediated by the microbiota and associated with regulation of gene expression.

Gates, Leah A / Reis, Bernardo Sgarbi / Lund, Peder J / Paul, Matthew R / Leboeuf, Marylene / Djomo, Annaelle M / Nadeem, Zara / Lopes, Mariana / Vitorino, Francisca N / Unlu, Gokhan / Carroll, Thomas S / Birsoy, Kivanç / Garcia, Benjamin A / Mucida, Daniel / Allis, C David

Nature metabolism

2024 Volume 6, Issue 4, Page(s) 697–707

Abstract: Post-translational modifications (PTMs) on histones are a key source of regulation on chromatin through impacting cellular processes, including gene ... ...

Abstract	Post-translational modifications (PTMs) on histones are a key source of regulation on chromatin through impacting cellular processes, including gene expression
MeSH term(s)	Animals ; Histones/metabolism ; Mice ; Gastrointestinal Microbiome ; Gene Expression Regulation ; Female ; Protein Processing, Post-Translational ; Intestinal Mucosa/metabolism ; Acetylation ; Intestines/microbiology ; Triglycerides/metabolism ; Mice, Inbred C57BL
Chemical Substances	Histones ; tributyrin (S05LZ624MF) ; Triglycerides
Language	English
Publishing date	2024-02-27
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	2522-5812
ISSN (online)	2522-5812
DOI	10.1038/s42255-024-00992-2
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Article ; Online: Stable isotope tracing in vivo reveals a metabolic bridge linking the microbiota to host histone acetylation.

Lund, Peder J / Gates, Leah A / Leboeuf, Marylene / Smith, Sarah A / Chau, Lillian / Lopes, Mariana / Friedman, Elliot S / Saiman, Yedidya / Kim, Min Soo / Shoffler, Clarissa A / Petucci, Christopher / Allis, C David / Wu, Gary D / Garcia, Benjamin A

Cell reports

2022 Volume 41, Issue 11, Page(s) 111809

Abstract: The gut microbiota influences acetylation on host histones by fermenting dietary fiber into butyrate. Although butyrate could promote histone acetylation by inhibiting histone deacetylases, it may also undergo oxidation to acetyl-coenzyme A (CoA), a ... ...

Abstract	The gut microbiota influences acetylation on host histones by fermenting dietary fiber into butyrate. Although butyrate could promote histone acetylation by inhibiting histone deacetylases, it may also undergo oxidation to acetyl-coenzyme A (CoA), a necessary cofactor for histone acetyltransferases. Here, we find that epithelial cells from germ-free mice harbor a loss of histone H4 acetylation across the genome except at promoter regions. Using stable isotope tracing in vivo with
MeSH term(s)	Mice ; Animals ; Acetylation ; Histones/metabolism ; Histone Acetyltransferases/metabolism ; Isotopes/metabolism ; Microbiota ; Carbon/metabolism ; Butyrates ; Colitis ; Fatty Acids
Chemical Substances	Histones ; Histone Acetyltransferases (EC 2.3.1.48) ; Isotopes ; Carbon (7440-44-0) ; Butyrates ; Fatty Acids
Language	English
Publishing date	2022-12-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.111809
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Article ; Online: CDKN1A regulates Langerhans cell survival and promotes Treg cell generation upon exposure to ionizing irradiation.

Price, Jeremy G / Idoyaga, Juliana / Salmon, Hélène / Hogstad, Brandon / Bigarella, Carolina L / Ghaffari, Saghi / Leboeuf, Marylene / Merad, Miriam

Nature immunology

2015 Volume 16, Issue 10, Page(s) 1060–1068

Abstract: Treatment with ionizing radiation (IR) can lead to the accumulation of tumor-infiltrating regulatory T cells (Treg cells) and subsequent resistance of tumors to radiotherapy. Here we focused on the contribution of the epidermal mononuclear phagocytes ... ...

Abstract	Treatment with ionizing radiation (IR) can lead to the accumulation of tumor-infiltrating regulatory T cells (Treg cells) and subsequent resistance of tumors to radiotherapy. Here we focused on the contribution of the epidermal mononuclear phagocytes Langerhans cells (LCs) to this phenomenon because of their ability to resist depletion by high-dose IR. We found that LCs resisted apoptosis and rapidly repaired DNA damage after exposure to IR. In particular, we found that the cyclin-dependent kinase inhibitor CDKN1A (p21) was overexpressed in LCs and that Cdkn1a(-/-) LCs underwent apoptosis and accumulated DNA damage following IR treatment. Wild-type LCs upregulated major histocompatibility complex class II molecules, migrated to the draining lymph nodes and induced an increase in Treg cell numbers upon exposure to IR, but Cdkn1a(-/-) LCs did not. Our findings suggest a means for manipulating the resistance of LCs to IR to enhance the response of cutaneous tumors to radiotherapy.
MeSH term(s)	Animals ; Cell Survival/genetics ; Cell Survival/radiation effects ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p21/genetics ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Flow Cytometry ; Langerhans Cells/radiation effects ; Mice ; Microarray Analysis ; Polymerase Chain Reaction ; Radiation, Ionizing ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/radiation effects ; Up-Regulation
Chemical Substances	Cyclin-Dependent Kinase Inhibitor p21
Language	English
Publishing date	2015-09-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/ni.3270
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Zs.A 5294: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 42: Show issues

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Article ; Online: Requirement for innate immunity and CD90⁺ NK1.1⁻ lymphocytes to treat established melanoma with chemo-immunotherapy.

Moskalenko, Marina / Pan, Michael / Fu, Yichun / de Moll, Ellen H / Hashimoto, Daigo / Mortha, Arthur / Leboeuf, Marylene / Jayaraman, Padmini / Bernardo, Sebastian / Sikora, Andrew G / Wolchok, Jedd / Bhardwaj, Nina / Merad, Miriam / Saenger, Yvonne

Cancer immunology research

2015 Volume 3, Issue 3, Page(s) 296–304

Abstract: We sought to define cellular immune mechanisms of synergy between tumor-antigen-targeted monoclonal antibodies and chemotherapy. Established B16 melanoma in mice was treated with cytotoxic doses of cyclophosphamide in combination with an antibody ... ...

Abstract	We sought to define cellular immune mechanisms of synergy between tumor-antigen-targeted monoclonal antibodies and chemotherapy. Established B16 melanoma in mice was treated with cytotoxic doses of cyclophosphamide in combination with an antibody targeting tyrosinase-related protein 1 (αTRP1), a native melanoma differentiation antigen. We find that Fcγ receptors are required for efficacy, showing that antitumor activity of combination therapy is immune mediated. Rag1(-/-) mice deficient in adaptive immunity are able to clear tumors, and thus innate immunity is sufficient for efficacy. Furthermore, previously treated wild-type mice are not significantly protected against tumor reinduction, as compared with mice inoculated with irradiated B16 alone, consistent with a primarily innate immune mechanism of action of chemo-immunotherapy. In contrast, mice deficient in both classical natural killer (NK) lymphocytes and nonclassical innate lymphocytes (ILC) due to deletion of the IL2 receptor common gamma chain IL2γc(-/-)) are refractory to chemo-immunotherapy. Classical NK lymphocytes are not critical for treatment, as depletion of NK1.1⁺ cells does not impair antitumor effect. Depletion of CD90⁺NK1.1⁻ lymphocytes, however, both diminishes therapeutic benefit and decreases accumulation of macrophages within the tumor. Tumor clearance during combination chemo-immunotherapy with monoclonal antibodies against native antigen is mediated by the innate immune system. We highlight a novel potential role for CD90⁺NK1.1⁻ ILCs in chemo-immunotherapy.
MeSH term(s)	Adaptive Immunity ; Animals ; Antibodies, Monoclonal/therapeutic use ; Antigens, Ly/metabolism ; CD8-Positive T-Lymphocytes/immunology ; Cell Line, Tumor ; Cyclophosphamide/therapeutic use ; Female ; Immunity, Innate ; Immunotherapy ; Killer Cells, Natural/immunology ; Melanoma, Experimental/drug therapy ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NK Cell Lectin-Like Receptor Subfamily B/metabolism ; Oxidoreductases/immunology ; Receptors, IgG/immunology ; Thy-1 Antigens/metabolism
Chemical Substances	Antibodies, Monoclonal ; Antigens, Ly ; Klrb1c protein, mouse ; NK Cell Lectin-Like Receptor Subfamily B ; Receptors, IgG ; Thy-1 Antigens ; Cyclophosphamide (8N3DW7272P) ; Oxidoreductases (EC 1.-) ; tyrosinase-related protein-1 (EC 1.14.18.-)
Language	English
Publishing date	2015-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-14-0120
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Article ; Online: Epigenetic modulation of inflammation and synaptic plasticity promotes resilience against stress in mice.

Nature communications

2018 Volume 9, Issue 1, Page(s) 477

Abstract: Major depressive disorder is associated with abnormalities in the brain and the immune system. Chronic stress in animals showed that epigenetic and inflammatory mechanisms play important roles in mediating resilience and susceptibility to depression. ... ...

Abstract	Major depressive disorder is associated with abnormalities in the brain and the immune system. Chronic stress in animals showed that epigenetic and inflammatory mechanisms play important roles in mediating resilience and susceptibility to depression. Here, through a high-throughput screening, we identify two phytochemicals, dihydrocaffeic acid (DHCA) and malvidin-3'-O-glucoside (Mal-gluc) that are effective in promoting resilience against stress by modulating brain synaptic plasticity and peripheral inflammation. DHCA/Mal-gluc also significantly reduces depression-like phenotypes in a mouse model of increased systemic inflammation induced by transplantation of hematopoietic progenitor cells from stress-susceptible mice. DHCA reduces pro-inflammatory interleukin 6 (IL-6) generations by inhibiting DNA methylation at the CpG-rich IL-6 sequences introns 1 and 3, while Mal-gluc modulates synaptic plasticity by increasing histone acetylation of the regulatory sequences of the Rac1 gene. Peripheral inflammation and synaptic maladaptation are in line with newly hypothesized clinical intervention targets for depression that are not addressed by currently available antidepressants.
MeSH term(s)	Animals ; Anthocyanins/administration & dosage ; Anthocyanins/pharmacology ; Caffeic Acids/administration & dosage ; Caffeic Acids/pharmacology ; CpG Islands/drug effects ; Depression/drug therapy ; Drug Evaluation, Preclinical/methods ; Epigenesis, Genetic ; Glucosides/administration & dosage ; Glucosides/pharmacology ; Inflammation/genetics ; Interleukin-6/antagonists & inhibitors ; Interleukin-6/genetics ; Leukocyte Common Antigens/genetics ; Male ; Mice, Inbred C57BL ; Neuronal Plasticity/drug effects ; Neuronal Plasticity/genetics ; Neuropeptides/genetics ; Neuropeptides/metabolism ; Polyphenols/pharmacology ; Social Behavior ; Stress, Psychological/drug therapy ; Stress, Psychological/genetics ; rac1 GTP-Binding Protein/genetics ; rac1 GTP-Binding Protein/metabolism
Chemical Substances	Anthocyanins ; Caffeic Acids ; Glucosides ; Interleukin-6 ; Neuropeptides ; Polyphenols ; Rac1 protein, mouse ; interleukin-6, mouse ; 3,4-dihydroxyphenylpropionic acid (1078-61-1) ; malvidin-3-glucoside (7228-78-6) ; Leukocyte Common Antigens (EC 3.1.3.48) ; Ptprc protein, mouse (EC 3.1.3.48) ; rac1 GTP-Binding Protein (EC 3.6.5.2)
Language	English
Publishing date	2018-02-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-017-02794-5
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Article ; Online: Langerhans cell homeostasis and turnover after nonmyeloablative and myeloablative allogeneic hematopoietic cell transplantation.

Mielcarek, Marco / Kirkorian, Anna Yasmine / Hackman, Robert C / Price, Jeremy / Storer, Barry E / Wood, Brent L / Leboeuf, Marylene / Bogunovic, Milena / Storb, Rainer / Inamoto, Yoshihiro / Flowers, Mary E / Martin, Paul J / Collin, Matthew / Merad, Miriam

Transplantation

2014 Volume 98, Issue 5, Page(s) 563–568

Abstract: Background: Langerhans cells (LCs) are self-renewing epidermal myeloid cells that can migrate and mature into dendritic cells. Recipient LCs that survive cytotoxic therapy given in preparation for allogeneic hematopoietic cell transplantation may prime ... ...

Abstract	Background: Langerhans cells (LCs) are self-renewing epidermal myeloid cells that can migrate and mature into dendritic cells. Recipient LCs that survive cytotoxic therapy given in preparation for allogeneic hematopoietic cell transplantation may prime donor T cells to mediate cutaneous graft-versus-host disease (GVHD). This possible association, however, has not been investigated in the setting of nonmyeloablative allografting. Methods: We prospectively studied the kinetics of LC-chimerism after sex-mismatched allogeneic hematopoietic cell transplantation with nonmyeloablative (n=23) or myeloablative (n=25) conditioning. Combined XY-FISH and Langerin-staining was used to assess donor LC-chimerism in skin biopsies obtained on days 28, 56, and 84 after transplant. The degree of donor LC-chimerism was correlated with the development of skin GVHD. Results: We observed significantly delayed donor LC-engraftment after nonmyeloablative transplantation compared with other hematopoietic compartments and compared with LC-engraftment after myeloablative conditioning. In most recipients of nonmyeloablative transplants, recipient LCs proliferated in situ, recruitment of donor-LCs was delayed by two months, and full donor LC-chimerism was only reached by day 84 after transplant. Although persistence of host LCs on day-28 after transplant was not predictive for acute or chronic skin GVHD, the recruitment of donor-derived LCs was associated with nonspecific inflammatory infiltrates (P=0.009). Conclusions: These results show that LCs can self-renew locally but are replaced by circulating precursors even after minimally toxic nonmyeloablative transplant conditioning. Cutaneous inflammation accompanies donor LC-engraftment, but differences in LC conversion-kinetics do not predict clinical or histopathological GVHD.
MeSH term(s)	Adult ; Aged ; Female ; Graft vs Host Disease/etiology ; Graft vs Host Disease/prevention & control ; Hematopoietic Stem Cell Transplantation/methods ; Homeostasis ; Humans ; In Situ Hybridization, Fluorescence ; Langerhans Cells/physiology ; Male ; Middle Aged ; Prospective Studies ; Transplantation Chimera ; Transplantation Conditioning/methods ; Transplantation, Homologous/methods
Language	English
Publishing date	2014-04-09
Publishing country	United States
Document type	Clinical Trial ; Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	208424-7
ISSN	1534-6080 ; 0041-1337
ISSN (online)	1534-6080
ISSN	0041-1337
DOI	10.1097/TP.0000000000000097
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Zs.A 488: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 509: Show issues

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Article ; Online: Central role of conventional dendritic cells in regulation of bone marrow release and survival of neutrophils.

Jiao, Jingjing / Dragomir, Ana-Cristina / Kocabayoglu, Peri / Rahman, Adeeb H / Chow, Andrew / Hashimoto, Daigo / Leboeuf, Marylene / Kraus, Thomas / Moran, Thomas / Carrasco-Avino, Gonzalo / Friedman, Scott L / Merad, Miriam / Aloman, Costica

Journal of immunology (Baltimore, Md. : 1950)

2014 Volume 192, Issue 7, Page(s) 3374–3382

Abstract: Neutrophils are the most abundant cell type in the immune system and play an important role in the innate immune response. Using a diverse range of mouse models with either defective dendritic cell (DC) development or conditional DC depletion, we provide ...

Abstract	Neutrophils are the most abundant cell type in the immune system and play an important role in the innate immune response. Using a diverse range of mouse models with either defective dendritic cell (DC) development or conditional DC depletion, we provide in vivo evidence indicating that conventional DCs play an important role in the regulation of neutrophil homeostasis. Flk2, Flt3L, and Batf3 knockout mice, which have defects in DC development, have increased numbers of liver neutrophils in the steady state. Conversely, neutrophil frequency is reduced in DC-specific PTEN knockout mice, which have an expansion of CD8(+) and CD103(+) DCs. In chimeric CD11c-DTR mice, conventional DC depletion results in a systemic increase of neutrophils in peripheral organs in the absence of histological inflammation or an increase in proinflammatory cytokines. This effect is also present in splenectomized chimeric CD11c-DTR mice and is absent in chimeric mice with 50% normal bone marrow. In chimeric CD11c-DTR mice, diphtheria toxin treatment results in enhanced neutrophil trafficking from the bone marrow into circulation and increased neutrophil recruitment. Moreover, there is an increased expression of chemokines/cytokines involved in neutrophil homeostasis and reduced neutrophil apoptosis. These data underscore the role of the DC pool in regulating the neutrophil compartment in nonlymphoid organs.
MeSH term(s)	Animals ; Apoptosis/genetics ; Apoptosis/immunology ; Basic-Leucine Zipper Transcription Factors/deficiency ; Basic-Leucine Zipper Transcription Factors/genetics ; Basic-Leucine Zipper Transcription Factors/immunology ; Bone Marrow/immunology ; Bone Marrow/metabolism ; Bone Marrow Transplantation ; CD11c Antigen/genetics ; CD11c Antigen/immunology ; CD11c Antigen/metabolism ; Cell Survival/genetics ; Cell Survival/immunology ; Cytokines/immunology ; Cytokines/metabolism ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Female ; Flow Cytometry ; Heparin-binding EGF-like Growth Factor ; Homeostasis/genetics ; Homeostasis/immunology ; Inflammation Mediators/immunology ; Inflammation Mediators/metabolism ; Intercellular Signaling Peptides and Proteins/genetics ; Intercellular Signaling Peptides and Proteins/immunology ; Intercellular Signaling Peptides and Proteins/metabolism ; Liver/immunology ; Liver/metabolism ; Membrane Proteins/deficiency ; Membrane Proteins/genetics ; Membrane Proteins/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Microscopy, Confocal ; Neutrophils/immunology ; Neutrophils/metabolism ; PTEN Phosphohydrolase/deficiency ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/immunology ; Repressor Proteins/deficiency ; Repressor Proteins/genetics ; Repressor Proteins/immunology ; fms-Like Tyrosine Kinase 3/deficiency ; fms-Like Tyrosine Kinase 3/genetics ; fms-Like Tyrosine Kinase 3/immunology
Chemical Substances	Basic-Leucine Zipper Transcription Factors ; CD11c Antigen ; Cytokines ; Hbegf protein, mouse ; Heparin-binding EGF-like Growth Factor ; Inflammation Mediators ; Intercellular Signaling Peptides and Proteins ; Membrane Proteins ; Repressor Proteins ; SNFT protein, mouse ; flt3 ligand protein ; Flt3 protein, mouse (EC 2.7.10.1) ; fms-Like Tyrosine Kinase 3 (EC 2.7.10.1) ; PTEN Phosphohydrolase (EC 3.1.3.67)
Language	English
Publishing date	2014-03-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
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.1300237
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Ud II Zs.37: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 28: Show issues

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Article ; Online: Antigen-specific Treg impair CD8(+) T-cell priming by blocking early T-cell expansion.

Chappert, Pascal / Leboeuf, Marylène / Rameau, Philippe / Lalfer, Mélanie / Desbois, Sabine / Liblau, Roland S / Danos, Olivier / Davoust, Jean M / Gross, David-Alexandre

European journal of immunology

2010 Volume 40, Issue 2, Page(s) 339–350

Abstract: Foxp3(+) Treg are crucial for the maintenance of self-tolerance and have been shown to control CD8(+) T-cell effector functions. In addition, Treg are thought to control the priming of CD8(+) T cells, which recognize the same antigens as Treg. Taking ... ...

Abstract	Foxp3(+) Treg are crucial for the maintenance of self-tolerance and have been shown to control CD8(+) T-cell effector functions. In addition, Treg are thought to control the priming of CD8(+) T cells, which recognize the same antigens as Treg. Taking advantage of our model of peripheral tolerance induction to influenza hemagglutinin (HA) after HA gene transfer, we found that HA-specific Treg suppress antigen-linked CTL responses through early blockade of CD8(+) T-cell expansion. Confronted with their cognate antigen, Treg expand more rapidly than CD8(+) T cells and are highly suppressive only during the initial stages of immune priming. They nullify HA-specific CD8(+) T-cell responses, local inflammatory responses and rejection of HA transduced cells. When HA gene transfer is performed with extensive tissue inflammation, HA-specific Treg are less effective but still reduce the frequency of newly primed HA-specific CD8(+) T cells and the ensuing frequency of memory CD8(+) T cells. Our results demonstrate that Treg control CTL priming in an antigen-specific manner at the level of T-cell expansion, highlighting how self-reactive Treg could prevent the induction of autoimmune responses through selective blockade of autoreactive T-cell proliferation.
MeSH term(s)	Animals ; Antigens/immunology ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Cell Differentiation ; Cell Proliferation ; Female ; Flow Cytometry ; H-2 Antigens/genetics ; H-2 Antigens/immunology ; H-2 Antigens/metabolism ; Hemagglutinin Glycoproteins, Influenza Virus/genetics ; Hemagglutinin Glycoproteins, Influenza Virus/immunology ; Hemagglutinin Glycoproteins, Influenza Virus/metabolism ; Histocompatibility Antigen H-2D ; Immunologic Memory/immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; T-Lymphocytes, Cytotoxic/cytology ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Cytotoxic/metabolism ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism
Chemical Substances	Antigens ; H-2 Antigens ; Hemagglutinin Glycoproteins, Influenza Virus ; Histocompatibility Antigen H-2D
Language	English
Publishing date	2010-02
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.200839107
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Zs.A 489: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Longitudinal tracking of human dendritic cells in murine models using magnetic resonance imaging.

Briley-Saebo, Karen C / Leboeuf, Marylene / Dickson, Stephen / Mani, Venkatesh / Fayad, Zahi A / Palucka, A Karolina / Banchereau, Jacques / Merad, Miriam

Magnetic resonance in medicine

2010 Volume 64, Issue 5, Page(s) 1510–1519

Abstract: Ex vivo generated dendritic cells are currently used to induce therapeutic immunity in solid tumors. Effective immune response requires dendritic cells to home and remain in lymphoid organs to allow for adequate interaction with T lymphocytes. The aim of ...

Abstract	Ex vivo generated dendritic cells are currently used to induce therapeutic immunity in solid tumors. Effective immune response requires dendritic cells to home and remain in lymphoid organs to allow for adequate interaction with T lymphocytes. The aim of the current study was to detect and track Feridex labeled human dendritic cells in murine models using magnetic resonance imaging. Human dendritic cells were incubated with Feridex and the effect of labeling on dendritic cells immune function was evaluated. Ex vivo dendritic cell phantoms were used to estimate sensitivity of the magnetic resonance methods and in vivo homing was evaluated after intravenous or subcutaneous injection. R2-maps of liver, spleen, and draining lymph nodes were obtained and inductively coupled plasma mass spectrometry or relaxometry methods were used to quantify the Feridex tissue concentrations. Correlations between in vivo R2 values and iron content were then determined. Feridex labeling did not affect dendritic cell maturation or function. Phantom results indicated that it was possible to detect 125 dendritic cells within a given slice. Strong correlation between in vivo R2* values and iron deposition was observed. Importantly, Feridex-labeled dendritic cells were detected in the spleen for up to 2 weeks postintravenous injection. This study suggests that magnetic resonance imaging may be used to longitudinally track Feridex-labeled human dendritic cells for up to 2 weeks after injection.
MeSH term(s)	Animals ; Cell Tracking ; Cells, Cultured ; Dendritic Cells/cytology ; Dendritic Cells/transplantation ; Humans ; Magnetic Resonance Imaging/methods ; Mice ; Mice, Inbred C57BL ; Mice, Knockout
Language	English
Publishing date	2010-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	605774-3
ISSN	1522-2594 ; 0740-3194
ISSN (online)	1522-2594
ISSN	0740-3194
DOI	10.1002/mrm.22519
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Zs.A 1959: Show issues

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Article: Antigen-specific Treg impair CD8⁺ T-cell priming by blocking early T-cell expansion

Chappert, Pascal / Leboeuf, Marylène / Rameau, Philippe / Lalfer, Mélanie / Desbois, Sabine / Liblau, Roland S / Danos, Olivier / Davoust, Jean M / Gross, David-Alexandre

European journal of immunology. 2010 Feb., v. 40, no. 2

2010

Abstract: Foxp3⁺ Treg are crucial for the maintenance of self-tolerance and have been shown to control CD8⁺ T-cell effector functions. In addition, Treg are thought to control the priming of CD8⁺ T cells, which recognize the same antigens as Treg. Taking advantage ...

Abstract	Foxp3⁺ Treg are crucial for the maintenance of self-tolerance and have been shown to control CD8⁺ T-cell effector functions. In addition, Treg are thought to control the priming of CD8⁺ T cells, which recognize the same antigens as Treg. Taking advantage of our model of peripheral tolerance induction to influenza hemagglutinin (HA) after HA gene transfer, we found that HA-specific Treg suppress antigen-linked CTL responses through early blockade of CD8⁺ T-cell expansion. Confronted with their cognate antigen, Treg expand more rapidly than CD8⁺ T cells and are highly suppressive only during the initial stages of immune priming. They nullify HA-specific CD8⁺ T-cell responses, local inflammatory responses and rejection of HA transduced cells. When HA gene transfer is performed with extensive tissue inflammation, HA-specific Treg are less effective but still reduce the frequency of newly primed HA-specific CD8⁺ T cells and the ensuing frequency of memory CD8⁺ T cells. Our results demonstrate that Treg control CTL priming in an antigen-specific manner at the level of T-cell expansion, highlighting how self-reactive Treg could prevent the induction of autoimmune responses through selective blockade of autoreactive T-cell proliferation.
Language	English
Dates of publication	2010-02
Size	p. 339-350.
Publishing place	Wiley-VCH Verlag
Document type	Article
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.200839107
Database	NAL-Catalogue (AGRICOLA)

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