ADRB3 stimulation induced M2-like phenotype in in vitro primary human macrophages

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ADRB3 stimulation induced M2-like phenotype in in

vitro primary human macrophages

Tatiana Lopez, H. Zhang, Fabrice Neiers, E. Bouysse, Maeva Wendremaire,

Carmen Garrido, Frederic Lirussi

To cite this version:

Tatiana Lopez, H. Zhang, Fabrice Neiers, E. Bouysse, Maeva Wendremaire, et al.. ADRB3 stimulation induced M2-like phenotype in in vitro primary human macrophages. 17. International Congress of Immunology (IUIS 2019), Oct 2019, Beijin, China. 1 p., �10.1002/eji.201970400�. �hal-02735017�

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Abstracts of IUIS 2019 Beijing

17th International Congress of

Immunology

19-23 October 2019

Beijing, China

European Journal of Immunology Volume 49, Suppl. 3, October, 2019

This abstract book can be searched using the PDF search function to look, for example, for the Abstract number or author name

To cite an Abstract, please use the following format:

Abstract title. Authors. Conference: 17th International Congress of Immunology. Location Beijing, China. Date October 19-23, 2019. Eur. J. Immunol. 2019. 49, S3, page number(s). Meeting Abstract number [the Abstract number can be found above the title]

Disclaimer:

This abstract book has been produced using author-supplied copy.

No responsibility is assumed for any claims, instructions, methods or drug dosages contained in the abstracts; it is recommended that these are verified independently.

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Eur. J. Immunol. 2019. 49 (Suppl. 3): 1–2223 Abstracts

DOI: 10.1002/eji.201970400

TABLE OF CONTENTS

ANTIGEN PROCESSING AND PRESENTATION ... 4

IMMUNE RECEPTOR SIGNALING ... 18

INNATE RECEPTORS AND SIGNALING ... 41

CO-INHIBITORY MOLECULES AND RECEPTORS ... 89

CYTOKINES, CHEMOKINES AND RECEPTORS ... 108

COMPLEMENT AND RECEPTORS ... 172

INFLAMMASOME AND IMMUNITY ... 185

GLYCOIMMUNOLOGY ... 234

NON-CODING RNAS IN IMMUNE REGULATION ... 240

IMMUNOGENETICS AND IMMUNOEPIGENETICS ... 285

B CELL DEVELOPMENT AND ACTIVATION ... 313

T CELL DEVELOPMENT AND ACTIVATION ... 344

CYTOTOXIC T LYMPHOCYTES ... 386

HELPER T CELLS AND SUBSETS ... 403

INNATE LYMPHOID CELLS ... 428

NK CELLS AND INVARIANT T CELLS ... 447

MACROPHAGES AND DENDRITIC CELLS ... 480

GRANULOCYTES AND MAST CELLS ... 567

CELL DEATH, IMMUNITY AND INFLAMMATION ... 590

IMMUNE CELL TRAFFICKING AND HOMING ... 643

REGULATORY IMMUNE CELLS AND IMMUNE REGULATION ... 653

IMMUNOLOGICAL MEMORY ... 707

ALLERGY ... 720

AUTOIMMUNE DISEASE ... 760

IMMUNITY TO VIRUSES ... 987

IMMUNITY TO BACTERIA ... 1105

IMMUNITY TO FUNGI AND PARASITES ... 1169

IMMUNODEFICIENCY ... 1219

IMMUNE SUPRESSION, TOLERANCE AND EXHAUSTION ... 1242

IMMUNOMETABOLISM ... 1276

MICROBIOME AND IMMUNE SYSTEM ... 1317

SYSTEMS BIOLOGY AND IMMUNOLOGY ... 1342

MUCOSAL IMMUNOLOGY ... 1350

REGIONAL IMMUNOLOGY AND DISEASE ... 1394

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Abstracts

DOI: 10.1002/eji.201970400

NEUROIMMUNOLOGY ... 1425

TRANSPLANTATION ... 1469

TUMOR ANTIGENS AND ESCAPE MECHANISMS ... 1514

REPRODUCTIVE IMMUNOLOGY ... 1594

VETERINARY AND COMPARATIVE IMMUNOLOGY ... 1624

VACCINES FOR INFECTION AND CANCER ... 1642

CAR ENGINEERED IMMUNE CELLS ... 1710

CHECKPOINT BLOCKADE AND ANTIBODY THERAPY ... 1730

ADOPTIVE CELL THERAPY ... 1785

CYTOKINE ANTAGONISTS IN THERAPY ... 1810

ADJUVANT AND DELIVERY SYSTEM ... 1819

IMMUNOPHARMACOLOGY ... 1836

TRADITIONAL MEDICINE AND IMMUNITY ... 1882

EMERGING TECHNIQUES AND TARGETS IN IMMUNE DIAGNOSIS ... 1948

GENE-EDITING IN IMMUNITY ... 1984

IMAGING OF IMMUNE SYSTEM ... 1990

OMICS AND BIOINFORMATICS IN IMMUNITY ... 1997

AUTHOR INDEX ... 2017

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Abstracts DOI: 10.1002/eji.201970400

performed by the same individual cells, but sequentially in time and in different micro-anatomical locations. In addition, we showed that TNF signaling promoted pDC IFN-I production. Hence, we propose a novel model of how individual pDC are endowed to exert different functions in vivo during a viral infection in a manner tightly orchestrated in time and space.

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ADRB3 stimulation induced M2-like phenotype in in vitro primary human macrophages

Lopez T.1_{, Zhang H.}1,2_{, Neiers F.}3_{, Bouysse E.}1_{, Wendremaire M.}1,4_{, Garrido C.}1_{, Lirussi F.}1,4

1_{INSERM LNC UMR 1231, Dijon, France,}2_{Department of Basic Medicine, College of Medicine,}

Hangzhou, China, the People's Republic, 3_{INRA UMR1324, Dijon, France,}4_{University Hospital of}

Dijon, Dijon, France

Background: Inflammatory bowel diseases (IBD) are a worldwide health-care problem with a continuously increasing incidence, caused by an impaired or inappropriate inflammatory response toward intestinal bacteria that is mainly headed by the recruitment of inflammatory macrophages. Among environmental factors, stress, via the secretion of cathecholamines, has been shown to activate catecholaminergic receptors. a-adrenoreceptors boost inflammation/oxidative stress while b2-adrenergic (b2-AR) signaling suppresses immunity. We demonstrated that b3-AR, is also expressed and functional in human macrophages. Thus, the investigation of b3-AR pathway could be of interest for the treatment of IBD.

Methods: In this study we characterized macrophages maturation status after in vitro stimulation with 3-agonists and identify the signalling pathways induced.

Results: Using flow cytometry, we showed that b3-AR stimulation leads to inflammatory and anti-oxidant responses, polarizing macrophages toward a M2-like phenotype. Cell surface marker CD206 is upregulated for 2 ± 0,24 fold (p< 0.05) while HLA-DR is down-regulated for 1.4 ± 0.3 fold (p< 0.05) after b3-AR stimulation compared to control group. We also demonstrated that these effects depend upon an ERK1/2- activation. Finally, we showed that b3-AR is resistant to desensitization thanks to a Gs/Gi switch and can induce its own expression after long term stimulation since we showed an overexpression of ADRB3 (2 to 3 ± 0.6 fold p< 0.05) and a 6 to 8 ± 1.7 log2-fold increase (p< 0.05) of mRNAADRB3 expression after 24 hours of treatment.

Conclusion: These preliminary results suggest that the use of b3-agonists may be of interest for the pharmacological managementof IBD.

P1930

mTORC1 promotes the differentiation of bone marrow-derived dendritic cells via

Stat3/Smad3/Id2 axis

Haojie W., Yuefang L., Jing D., Yujiao M., Hui W., Sheng X., Xia L., Xiaoming Z., Qixiang S.

Jiangsu University, Department of Immunology, School of Medicine, Zhenjiang, China, the People's Republic

Dendritic cells (DCs) are important antigen presenting cells (APCs) and play a crucial role in the regulation of immune responses. Previous reports have found that mTOR is involved in DCs differentiation, and inhibitor of DNA-binding protein 2 (Id2) has a close relationship with the

differentiation of DCs. However, the exact mechanism between them has not been fully elucidated. Here we demonstrated that rapamycin (RAPA), an inhibitor of mTOR, represses the maturation of bone marrow-derived DCs (BMDCs) via inhibiting the expression of Id2. By direct interacting with Stat3, mTORC1 up-regulates the activity of Stat3, thereby inhibiting the nuclear translocation and phosphorylation of Smad3. The phosphorylated Smad3 promotes the degradation of Id2 via activating Eur. J. Immunol. 2019. 49 (Suppl. 3): 1 2223