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Article ; Online: Antigen receptor-engineered Tregs inhibit CNS autoimmunity in cell therapy using nonredundant immune mechanisms in mice.

Pohar, Jelka / O'Connor, Richard / Manfroi, Benoît / El-Behi, Mohamed / Jouneau, Luc / Boudinot, Pierre / Bunse, Mario / Uckert, Wolfgang / Luka, Marine / Ménager, Mickael / Liblau, Roland / Anderton, Stephen M / Fillatreau, Simon

European journal of immunology

2022 Volume 52, Issue 8, Page(s) 1335–1349

Abstract: ... ...

Abstract	CD4
MeSH term(s)	Animals ; Autoimmunity ; CTLA-4 Antigen ; Cell- and Tissue-Based Therapy ; Forkhead Transcription Factors/genetics ; Immune System Diseases ; Interleukin-10 ; Mice ; Receptors, Antigen ; T-Lymphocytes, Regulatory
Chemical Substances	CTLA-4 Antigen ; Forkhead Transcription Factors ; Receptors, Antigen ; Interleukin-10 (130068-27-8)
Language	English
Publishing date	2022-05-27
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.202249845
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Article ; Online: Analysis of Microglia and Monocyte-derived Macrophages from the Central Nervous System by Flow Cytometry.

Martin, Elodie / El-Behi, Mohamed / Fontaine, Bertrand / Delarasse, Cecile

Journal of visualized experiments : JoVE

2017 , Issue 124

Abstract: Numerous studies have demonstrated the role of immune cells, in particular macrophages, in central nervous system (CNS) pathologies. There are two main macrophage populations in the CNS: (i) the microglia, which are the resident macrophages of the CNS ... ...

Abstract	Numerous studies have demonstrated the role of immune cells, in particular macrophages, in central nervous system (CNS) pathologies. There are two main macrophage populations in the CNS: (i) the microglia, which are the resident macrophages of the CNS and are derived from yolk sac progenitors during embryogenesis, and (ii) the monocyte-derived macrophages (MDM), which can infiltrate the CNS during disease and are derived from bone marrow progenitors. The roles of each macrophage subpopulation differ depending on the pathology being studied. Furthermore, there is no consensus on the histological markers or the distinguishing criteria used for these macrophage subpopulations. However, the analysis of the expression profiles of the CD11b and CD45 markers by flow cytometry allows us to distinguish the microglia (CD11b
MeSH term(s)	Animals ; Biomarkers/analysis ; CD11b Antigen/biosynthesis ; Central Nervous System/cytology ; Central Nervous System/immunology ; Flow Cytometry/methods ; Leukocyte Common Antigens/biosynthesis ; Macrophages/cytology ; Macrophages/immunology ; Mice ; Microglia/cytology ; Microglia/immunology
Chemical Substances	Biomarkers ; CD11b Antigen ; Leukocyte Common Antigens (EC 3.1.3.48) ; Ptprc protein, mouse (EC 3.1.3.48)
Language	English
Publishing date	2017-06-22
Publishing country	United States
Document type	Journal Article ; Video-Audio Media
ISSN	1940-087X
ISSN (online)	1940-087X
DOI	10.3791/55781
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Article ; Online: AKT activity orchestrates marginal zone B cell development in mice and humans.

Cox, Eva-Maria / El-Behi, Mohamed / Ries, Stefanie / Vogt, Johannes F / Kohlhaas, Vivien / Michna, Thomas / Manfroi, Benoît / Al-Maarri, Mona / Wanke, Florian / Tirosh, Boaz / Pondarre, Corinne / Lezeau, Harry / Yogev, Nir / Mittenzwei, Romy / Descatoire, Marc / Weller, Sandra / Weill, Jean-Claude / Reynaud, Claude-Agnès / Boudinot, Pierre /

Jouneau, Luc / Tenzer, Stefan / Distler, Ute / Rensing-Ehl, Anne / König, Christoph / Staniek, Julian / Rizzi, Marta / Magérus, Aude / Rieux-Laucat, Frederic / Wunderlich, F Thomas / Hövelmeyer, Nadine / Fillatreau, Simon

Cell reports

2023 Volume 42, Issue 4, Page(s) 112378

Abstract: The signals controlling marginal zone (MZ) and follicular (FO) B cell development remain incompletely understood. Here, we show that AKT orchestrates MZ B cell formation in mice and humans. Genetic models that increase AKT signaling in B cells or abolish ...

Abstract	The signals controlling marginal zone (MZ) and follicular (FO) B cell development remain incompletely understood. Here, we show that AKT orchestrates MZ B cell formation in mice and humans. Genetic models that increase AKT signaling in B cells or abolish its impact on FoxO transcription factors highlight the AKT-FoxO axis as an on-off switch for MZ B cell formation in mice. In humans, splenic immunoglobulin (Ig) D
MeSH term(s)	Humans ; Mice ; Animals ; Proto-Oncogene Proteins c-akt ; B-Lymphocytes ; Lymphoid Tissue ; Signal Transduction ; Spleen
Chemical Substances	Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2023-04-14
Publishing country	United States
Document type	Journal Article ; 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.2023.112378
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Article ; Online: Current views on the roles of Th1 and Th17 cells in experimental autoimmune encephalomyelitis.

El-behi, Mohamed / Rostami, Abdolmohamad / Ciric, Bogoljub

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2010 Volume 5, Issue 2, Page(s) 189–197

Abstract: Multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), are autoimmune demyelinating diseases of the central nervous system (CNS). Interferon-gamma-producing Th1 and interleukin-17-producing Th17 CD4(+) T helper (Th) ...

Abstract	Multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), are autoimmune demyelinating diseases of the central nervous system (CNS). Interferon-gamma-producing Th1 and interleukin-17-producing Th17 CD4(+) T helper (Th) cells mediate disease pathogenesis in EAE and likely in MS as well. However, the relative contribution of each Th subset to autoimmune processes in the CNS remains unclear. Emerging data suggest that both Th1 and Th17 cells contribute to CNS autoimmunity, albeit through different mechanisms. A better understanding of the roles that Th1 and Th17 cells play in autoimmune inflammation will be helpful in developing new therapeutic approaches. In this review, we discuss recent findings on the roles of Th1 and Th17 cells in the pathogenesis of EAE.
MeSH term(s)	Animals ; CD4-Positive T-Lymphocytes/metabolism ; CD4-Positive T-Lymphocytes/physiology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Humans ; Interleukin-17/biosynthesis ; Interleukin-17/physiology ; Interleukin-23/physiology ; Receptors, Chemokine/physiology ; Th1 Cells/metabolism ; Th1 Cells/physiology
Chemical Substances	Interleukin-17 ; Interleukin-23 ; Receptors, Chemokine
Language	English
Publishing date	2010-01-27
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-009-9188-9
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Article: Epidemiological and Phylogeographic Study of Equid Herpesviruses in Tunisia.

Badr, Chaima / Souiai, Oussama / Arbi, Marwa / El Behi, Imen / Essaied, Mohamed S / Khosrof, Ines / Benkahla, Alia / Chabchoub, Ahmed / Ghram, Abdeljelil

Pathogens (Basel, Switzerland)

2022 Volume 11, Issue 9

Abstract: Equid herpesvirus (EHV) is a contagious viral disease affecting horses, causing illness characterized by respiratory symptoms, abortion and neurological disorders. It is common worldwide and causes severe economic losses to the equine industry. The ... ...

Abstract	Equid herpesvirus (EHV) is a contagious viral disease affecting horses, causing illness characterized by respiratory symptoms, abortion and neurological disorders. It is common worldwide and causes severe economic losses to the equine industry. The present study was aimed at investigating the incidence of EHVs, the genetic characterization of Tunisian isolates and a spatiotemporal study, using 298 collected samples from diseased and clinically healthy horses. The global incidence of EHV infection was found to be about 71.81%. EHV2 and EHV5 were detected in 146 (48.99%) and 159 (53.35%) sampled horses, respectively. EHV1 was detected in 11 samples (3.69%); EHV4 was not detected. Co-infections with EHV1-EHV2, EHV1-EHV5 and EHV2-EHV5 were observed in 0.33%, 1.34% and 31.54% of tested horses, respectively. Phylogenetic analyses showed that gB of EHV2 and EHV5 displays high genetic diversity with a nucleotide sequence identity ranging from 88 to 100% for EHV2 and 97.5 to 100% for EHV5. Phylogeography suggested Iceland and USA as the most likely countries of origin of the Tunisian EHV2 and EHV5 isolates. These viruses detected in Tunisia seemed to be introduced in the 2000s. This first epidemiological and phylogeographic study is important for better knowledge of the evolution of equid herpesvirus infections in Tunisia.
Language	English
Publishing date	2022-09-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2695572-6
ISSN	2076-0817
ISSN	2076-0817
DOI	10.3390/pathogens11091016
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Article: Analysis of microglia and monocyte-derived macrophages from the central nervous system by flow cytometry

Martin, Elodie / El-Behi, Mohamed / Fontaine, Bertrand / Delarasse, Cecile

Journal of visualized experiments. 2017 June 22, , no. 124

2017

Abstract	Numerous studies have demonstrated the role of immune cells, in particular macrophages, in central nervous system (CNS) pathologies. There are two main macrophage populations in the CNS: (i) the microglia, which are the resident macrophages of the CNS and are derived from yolk sac progenitors during embryogenesis, and (ii) the monocyte-derived macrophages (MDM), which can infiltrate the CNS during disease and are derived from bone marrow progenitors. The roles of each macrophage subpopulation differ depending on the pathology being studied. Furthermore, there is no consensus on the histological markers or the distinguishing criteria used for these macrophage subpopulations. However, the analysis of the expression profiles of the CD11b and CD45 markers by flow cytometry allows us to distinguish the microglia (CD11b+CD45med) from the MDM (CD11b+CD45high). In this protocol, we show that the density gradient centrifugation and the flow cytometry analysis can be used to characterize these CNS macrophage subpopulations, and to study several markers of interest expressed by these cells as we recently published. Thus, this technique can further our understanding of the role of macrophages in mouse models of neurological diseases and can also be used to evaluate drug effects on these cells.
Keywords	animal models ; bone marrow ; central nervous system ; density gradient centrifugation ; drugs ; embryogenesis ; flow cytometry ; histology ; macrophages ; nervous system diseases ; neuroglia ; yolk sac
Language	English
Dates of publication	2017-0622
Size	p. e55781.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/55781
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: AKT activity orchestrates marginal zone B cell development in mice and humans

Eva-Maria Cox / Mohamed El-Behi / Stefanie Ries / Johannes F. Vogt / Vivien Kohlhaas / Thomas Michna / Benoît Manfroi / Mona Al-Maarri / Florian Wanke / Boaz Tirosh / Corinne Pondarre / Harry Lezeau / Nir Yogev / Romy Mittenzwei / Marc Descatoire / Sandra Weller / Jean-Claude Weill / Claude-Agnès Reynaud / Pierre Boudinot /

Luc Jouneau / Stefan Tenzer / Ute Distler / Anne Rensing-Ehl / Christoph König / Julian Staniek / Marta Rizzi / Aude Magérus / Frederic Rieux-Laucat / F. Thomas Wunderlich / Nadine Hövelmeyer / Simon Fillatreau

Cell Reports, Vol 42, Iss 4, Pp 112378- (2023)

2023

Abstract: Summary: The signals controlling marginal zone (MZ) and follicular (FO) B cell development remain incompletely understood. Here, we show that AKT orchestrates MZ B cell formation in mice and humans. Genetic models that increase AKT signaling in B cells ... ...

Abstract	Summary: The signals controlling marginal zone (MZ) and follicular (FO) B cell development remain incompletely understood. Here, we show that AKT orchestrates MZ B cell formation in mice and humans. Genetic models that increase AKT signaling in B cells or abolish its impact on FoxO transcription factors highlight the AKT-FoxO axis as an on-off switch for MZ B cell formation in mice. In humans, splenic immunoglobulin (Ig) D+CD27+ B cells, proposed as an MZ B cell equivalent, display higher AKT signaling than naive IgD+CD27− and memory IgD−CD27+ B cells and develop in an AKT-dependent manner from their precursors in vitro, underlining the conservation of this developmental pathway. Consistently, CD148 is identified as a receptor indicative of the level of AKT signaling in B cells, expressed at a higher level in MZ B cells than FO B cells in mice as well as humans.
Keywords	CP: Immunology ; CP: Developmental biology ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2023-04-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Committed Tc17 cells are phenotypically and functionally resistant to the effects of IL-27.

El-Behi, Mohamed / Dai, Hong / Magalhaes, Joao G / Hwang, Daniel / Zhang, Guang-Xian / Rostami, Abdolmohamad / Ciric, Bogoljub

European journal of immunology

2014 Volume 44, Issue 10, Page(s) 3003–3014

Abstract: IL-17-secreting CD8(+) T cells (Tc17 cells) have been implicated in immunity to infections, cancer, and autoimmune diseases. Thus far, studies on Tc17 cells have primarily investigated their development from naïve precursors, while the biology of ... ...

Abstract	IL-17-secreting CD8(+) T cells (Tc17 cells) have been implicated in immunity to infections, cancer, and autoimmune diseases. Thus far, studies on Tc17 cells have primarily investigated their development from naïve precursors, while the biology of committed Tc17 cells has been less characterized, in particular during the effector phase of immune responses. IL-27 is an important regulator of inflammation through the induction of regulatory Tr1 cells, as well as a suppressor of Th17-cell development. IL-27 suppresses the development of Tc17 cells, but its effects on committed Tc17 cells are unknown. Here we demonstrate that even though IL-27 completely inhibited the development of C57BL/6 mouse Tc17 cells, it had little effect on previously committed Tc17 cells. Although committed Tc17 cells were capable of responding to IL-27, it had no effect on expression of RORγt and RORα, or production of various cytokines. Committed Tc17 cells did not express granzyme B and lacked cytotoxicity in vitro, features that remained unaltered by IL-27 treatment. Nonetheless, they efficiently induced diabetes, irrespective of treatment with IL-27 prior to transfer into RIP-mOVA mice. These findings suggest that use of IL-27 to modulate autoimmune diseases might have limited therapeutic efficacy if autoaggressive Tc17 cells have already developed.
MeSH term(s)	Animals ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/drug effects ; CD8-Positive T-Lymphocytes/immunology ; Cell Differentiation/immunology ; Cell Lineage/immunology ; Flow Cytometry ; Interleukin-17/immunology ; Interleukin-17/metabolism ; Interleukin-27/immunology ; Interleukin-27/pharmacology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Phenotype ; Real-Time Polymerase Chain Reaction ; T-Lymphocyte Subsets/cytology ; T-Lymphocyte Subsets/drug effects ; T-Lymphocyte Subsets/immunology
Chemical Substances	Interleukin-17 ; Interleukin-27
Language	English
Publishing date	2014-01-31
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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.201344360
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Article ; Online: IL-23 drives pathogenic IL-17-producing CD8+ T cells.

Ciric, Bogoljub / El-behi, Mohamed / Cabrera, Rosalyn / Zhang, Guang-Xian / Rostami, Abdolmohamad

Journal of immunology (Baltimore, Md. : 1950)

2009 Volume 182, Issue 9, Page(s) 5296–5305

Abstract: IL-17-producing CD8(+) T cells (Tc17) appear to play a role in a range of conditions, such as autoimmunity and cancer. Thus far, Tc17 cells have been only marginally studied, resulting in a paucity of data on their biology and function. We demonstrate ... ...

Abstract	IL-17-producing CD8(+) T cells (Tc17) appear to play a role in a range of conditions, such as autoimmunity and cancer. Thus far, Tc17 cells have been only marginally studied, resulting in a paucity of data on their biology and function. We demonstrate that Tc17 and Th17 cells share similar developmental characteristics, including the previously unknown promoting effect of IL-21 on Tc17 cell differentiation and IL-23-dependent expression of IL-22. Both STAT1 and STAT4 are required for optimal development of Tc17 cells and maximal secretion of cytokines. Tc17 cells are cytotoxic, and they can be either pathogenic or nonpathogenic upon adoptive transfer in the model of autoimmune diabetes. Tc17 cells treated with TGF-beta1 plus IL-6 are not diabetogenic, whereas IL-23-treated cells potently induce the disease. IL-17A and IL-17F are necessary but not sufficient for diabetes induction by Tc17 cells. Tc17 cells treated with TGF-beta1 plus IL-6 or IL-23 likely differ in pathogenicity due to their disparate capacity to attract other immune cells and initiate inflammation.
MeSH term(s)	Animals ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/pathology ; Cell Line, Tumor ; Cells, Cultured ; Cytotoxicity Tests, Immunologic ; Diabetes Mellitus, Experimental/immunology ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/pathology ; Immunophenotyping ; Interleukin-17/biosynthesis ; Interleukin-17/metabolism ; Interleukin-17/physiology ; Interleukin-23/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Helper-Inducer/metabolism
Chemical Substances	Interleukin-17 ; Interleukin-23
Language	English
Publishing date	2009-04-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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.0900036
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Article ; Online: Differential effect of IL-27 on developing versus committed Th17 cells.

El-behi, Mohamed / Ciric, Bogoljub / Yu, Shuo / Zhang, Guang-Xian / Fitzgerald, Denise C / Rostami, Abdolmohamad

Journal of immunology (Baltimore, Md. : 1950)

2009 Volume 183, Issue 8, Page(s) 4957–4967

Abstract: IL-27 counters the effect of TGF-beta+IL-6 on naive CD4(+) T cells, resulting in near complete inhibition of de novo Th17 development. In contrast, little is known about the effect of IL-27 on already differentiated Th17 cells. A better understanding of ... ...

Abstract	IL-27 counters the effect of TGF-beta+IL-6 on naive CD4(+) T cells, resulting in near complete inhibition of de novo Th17 development. In contrast, little is known about the effect of IL-27 on already differentiated Th17 cells. A better understanding of how IL-27 regulates these cells is needed to evaluate the therapeutic potential of IL-27 in Th17 cells-associated diseases. In this study, we show that IL-27 had surprisingly little effect on committed Th17 cells, despite its expression of a functional IL-27R. Contrary to de novo differentiation of Th17 cells, IL-27 did not suppress expression of retinoid-related orphan receptor (ROR)gammat or RORalpha in committed Th17 cells. Consistent with this finding, the frequency of committed Th17 cells and their cytokine secretion remained unaffected by IL-27. Both memory Th17 cells (CD4(+)CD25(-)CD62L(low)) that developed in vivo and encephalitogenic Th17 cells infiltrating the CNS of mice developing experimental autoimmune encephalomyelitis produced similar amounts of IL-17A when reactivated with IL-23 in the absence and presence of exogenous IL-27. Finally, IL-27 failed to suppress encephalitogenicity of Th17 cells in an adoptive transfer of experimental autoimmune encephalomyelitis. Analysis ex vivo of transferred Th17 cells in the spleen and CNS of recipient mice showed that cells retained similar phenotype irrespective of whether cells were treated or not with IL-27. Our data demonstrate that in contrast to inhibition of de novo differentiation of Th17 cells, IL-27 has little or no effect on committed Th17 cells. These findings indicate that therapeutic applications of IL-27 might have a limited efficacy in inflammatory conditions where aggressive Th17 responses have already developed.
MeSH term(s)	Adoptive Transfer ; Animals ; Cytokines/biosynthesis ; Cytokines/immunology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Female ; Glycoproteins/immunology ; Interleukin-17/immunology ; Interleukins/immunology ; Interleukins/pharmacology ; Mice ; Mice, Inbred C57BL ; Myelin-Oligodendrocyte Glycoprotein ; Peptide Fragments/immunology ; Receptors, Cytokine/immunology ; Receptors, Cytokine/metabolism ; Receptors, Retinoic Acid/immunology ; Receptors, Retinoic Acid/metabolism ; STAT1 Transcription Factor/genetics ; STAT1 Transcription Factor/immunology ; STAT1 Transcription Factor/metabolism ; STAT3 Transcription Factor/immunology ; STAT3 Transcription Factor/metabolism ; T-Box Domain Proteins/genetics ; T-Box Domain Proteins/immunology ; T-Box Domain Proteins/metabolism ; T-Lymphocytes, Helper-Inducer/drug effects ; T-Lymphocytes, Helper-Inducer/immunology
Chemical Substances	Cytokines ; Glycoproteins ; Il17a protein, mouse ; Il27 protein, mouse ; Interleukin-17 ; Interleukins ; Myelin-Oligodendrocyte Glycoprotein ; Peptide Fragments ; Receptors, Cytokine ; Receptors, Retinoic Acid ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; Stat1 protein, mouse ; Stat3 protein, mouse ; T-Box Domain Proteins ; T-box transcription factor TBX21 ; myelin oligodendrocyte glycoprotein (35-55)
Language	English
Publishing date	2009-09-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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.0900735
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