D1-like dopamine receptors promote B-cell differentiation in systemic lupus erythematosus

Background Systemic lupus erythematosus (SLE) is an autoimmune disease that currently cannot be completely cured with a great health burden. Since the production of autoantibodies plays a key role in the pathogenesis of SLE, discovering the underlying immunoregulation mechanism of B cells will be he...
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Autor*in:	Xiang, Zhongyuan [verfasserIn] Wu, Fengxi [verfasserIn] He, Zhenghao [verfasserIn] Tan, Fen [verfasserIn] Hu, Haoran [verfasserIn] Zou, Chun [verfasserIn] Yi, Ping [verfasserIn] liu, Wenen [verfasserIn] Yang, Ming [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2024

Schlagwörter:	Systemic lupus erythematosus Dopamine receptor D1-like receptor B cell Therapeutic target

Anmerkung:	© The Author(s) 2024

Übergeordnetes Werk:	Enthalten in: Cell communication and signaling - BioMed Central, 2003, 22(2024), 1 vom: 17. Okt.
Übergeordnetes Werk:	volume:22 ; year:2024 ; number:1 ; day:17 ; month:10

Links:	Volltext

DOI / URN:	10.1186/s12964-024-01885-3

Katalog-ID:	SPR057846723

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520			\|a Background Systemic lupus erythematosus (SLE) is an autoimmune disease that currently cannot be completely cured with a great health burden. Since the production of autoantibodies plays a key role in the pathogenesis of SLE, discovering the underlying immunoregulation mechanism of B cells will be helpful for developing promising immunotherapy for SLE. In recent studies, dopamine receptors (DRDs), G protein-coupled receptors that include D1-like and D2-like subtypes, are expressed on B cells and participate in various physiological processes, involving immune responses. However, the regulatory effect of DRDs on B cells has not been determined. Methods This study explored the expression of DRDs on B-cell subsets from SLE patients and healthy individuals. The effects of D1-like receptor on B-cell activation and differentiation were further explored using D1-like receptor agonists or antagonists. RNA-seq and bioinformatics analyses were used to identify specific molecular mechanisms involved. Results The D1-like DRDs on B cells of SLE patients were highly expressed compared with those of healthy controls (HCs). D1-like receptor agonist treatment exacerbated lupus-like symptoms in pristane-induced lupus-like mice, while D1-like receptor antagonists alleviated the lupus-like phenotypes. Inhibition of D1-like receptor signals impeded B-cell differentiation, while activation of D1-like receptor signals could promote B cell differentiation. Further RNA-seq confirmed that PTGS2, a gene related to B-cell differentiation, was up-regulated once the D1-like receptor signals were activated, while BMP6 and IL-24 were up-regulated once the D1-like receptor signals were inhibited. Conclusion D1-like receptors probably promote B-cell differentiation through the PTGS2/PRDM1 pathway.
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allfields	10.1186/s12964-024-01885-3 doi (DE-627)SPR057846723 (SPR)s12964-024-01885-3-e DE-627 ger DE-627 rakwb eng 610 570 VZ 12 ssgn 42.15 bkl Xiang, Zhongyuan verfasserin aut D1-like dopamine receptors promote B-cell differentiation in systemic lupus erythematosus 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2024 Background Systemic lupus erythematosus (SLE) is an autoimmune disease that currently cannot be completely cured with a great health burden. Since the production of autoantibodies plays a key role in the pathogenesis of SLE, discovering the underlying immunoregulation mechanism of B cells will be helpful for developing promising immunotherapy for SLE. In recent studies, dopamine receptors (DRDs), G protein-coupled receptors that include D1-like and D2-like subtypes, are expressed on B cells and participate in various physiological processes, involving immune responses. However, the regulatory effect of DRDs on B cells has not been determined. Methods This study explored the expression of DRDs on B-cell subsets from SLE patients and healthy individuals. The effects of D1-like receptor on B-cell activation and differentiation were further explored using D1-like receptor agonists or antagonists. RNA-seq and bioinformatics analyses were used to identify specific molecular mechanisms involved. Results The D1-like DRDs on B cells of SLE patients were highly expressed compared with those of healthy controls (HCs). D1-like receptor agonist treatment exacerbated lupus-like symptoms in pristane-induced lupus-like mice, while D1-like receptor antagonists alleviated the lupus-like phenotypes. Inhibition of D1-like receptor signals impeded B-cell differentiation, while activation of D1-like receptor signals could promote B cell differentiation. Further RNA-seq confirmed that PTGS2, a gene related to B-cell differentiation, was up-regulated once the D1-like receptor signals were activated, while BMP6 and IL-24 were up-regulated once the D1-like receptor signals were inhibited. Conclusion D1-like receptors probably promote B-cell differentiation through the PTGS2/PRDM1 pathway. Systemic lupus erythematosus (dpeaa)DE-He213 Dopamine receptor (dpeaa)DE-He213 D1-like receptor (dpeaa)DE-He213 B cell (dpeaa)DE-He213 Therapeutic target (dpeaa)DE-He213 Wu, Fengxi verfasserin aut He, Zhenghao verfasserin aut Tan, Fen verfasserin aut Hu, Haoran verfasserin aut Zou, Chun verfasserin aut Yi, Ping verfasserin aut liu, Wenen verfasserin aut Yang, Ming verfasserin aut Enthalten in Cell communication and signaling BioMed Central, 2003 22(2024), 1 vom: 17. Okt. (DE-627)37375275X (DE-600)2126315-2 1478-811X nnns volume:22 year:2024 number:1 day:17 month:10 https://dx.doi.org/10.1186/s12964-024-01885-3 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 42.15 VZ AR 22 2024 1 17 10
spelling	10.1186/s12964-024-01885-3 doi (DE-627)SPR057846723 (SPR)s12964-024-01885-3-e DE-627 ger DE-627 rakwb eng 610 570 VZ 12 ssgn 42.15 bkl Xiang, Zhongyuan verfasserin aut D1-like dopamine receptors promote B-cell differentiation in systemic lupus erythematosus 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2024 Background Systemic lupus erythematosus (SLE) is an autoimmune disease that currently cannot be completely cured with a great health burden. Since the production of autoantibodies plays a key role in the pathogenesis of SLE, discovering the underlying immunoregulation mechanism of B cells will be helpful for developing promising immunotherapy for SLE. In recent studies, dopamine receptors (DRDs), G protein-coupled receptors that include D1-like and D2-like subtypes, are expressed on B cells and participate in various physiological processes, involving immune responses. However, the regulatory effect of DRDs on B cells has not been determined. Methods This study explored the expression of DRDs on B-cell subsets from SLE patients and healthy individuals. The effects of D1-like receptor on B-cell activation and differentiation were further explored using D1-like receptor agonists or antagonists. RNA-seq and bioinformatics analyses were used to identify specific molecular mechanisms involved. Results The D1-like DRDs on B cells of SLE patients were highly expressed compared with those of healthy controls (HCs). D1-like receptor agonist treatment exacerbated lupus-like symptoms in pristane-induced lupus-like mice, while D1-like receptor antagonists alleviated the lupus-like phenotypes. Inhibition of D1-like receptor signals impeded B-cell differentiation, while activation of D1-like receptor signals could promote B cell differentiation. Further RNA-seq confirmed that PTGS2, a gene related to B-cell differentiation, was up-regulated once the D1-like receptor signals were activated, while BMP6 and IL-24 were up-regulated once the D1-like receptor signals were inhibited. Conclusion D1-like receptors probably promote B-cell differentiation through the PTGS2/PRDM1 pathway. Systemic lupus erythematosus (dpeaa)DE-He213 Dopamine receptor (dpeaa)DE-He213 D1-like receptor (dpeaa)DE-He213 B cell (dpeaa)DE-He213 Therapeutic target (dpeaa)DE-He213 Wu, Fengxi verfasserin aut He, Zhenghao verfasserin aut Tan, Fen verfasserin aut Hu, Haoran verfasserin aut Zou, Chun verfasserin aut Yi, Ping verfasserin aut liu, Wenen verfasserin aut Yang, Ming verfasserin aut Enthalten in Cell communication and signaling BioMed Central, 2003 22(2024), 1 vom: 17. Okt. (DE-627)37375275X (DE-600)2126315-2 1478-811X nnns volume:22 year:2024 number:1 day:17 month:10 https://dx.doi.org/10.1186/s12964-024-01885-3 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 42.15 VZ AR 22 2024 1 17 10
allfields_unstemmed	10.1186/s12964-024-01885-3 doi (DE-627)SPR057846723 (SPR)s12964-024-01885-3-e DE-627 ger DE-627 rakwb eng 610 570 VZ 12 ssgn 42.15 bkl Xiang, Zhongyuan verfasserin aut D1-like dopamine receptors promote B-cell differentiation in systemic lupus erythematosus 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2024 Background Systemic lupus erythematosus (SLE) is an autoimmune disease that currently cannot be completely cured with a great health burden. Since the production of autoantibodies plays a key role in the pathogenesis of SLE, discovering the underlying immunoregulation mechanism of B cells will be helpful for developing promising immunotherapy for SLE. In recent studies, dopamine receptors (DRDs), G protein-coupled receptors that include D1-like and D2-like subtypes, are expressed on B cells and participate in various physiological processes, involving immune responses. However, the regulatory effect of DRDs on B cells has not been determined. Methods This study explored the expression of DRDs on B-cell subsets from SLE patients and healthy individuals. The effects of D1-like receptor on B-cell activation and differentiation were further explored using D1-like receptor agonists or antagonists. RNA-seq and bioinformatics analyses were used to identify specific molecular mechanisms involved. Results The D1-like DRDs on B cells of SLE patients were highly expressed compared with those of healthy controls (HCs). D1-like receptor agonist treatment exacerbated lupus-like symptoms in pristane-induced lupus-like mice, while D1-like receptor antagonists alleviated the lupus-like phenotypes. Inhibition of D1-like receptor signals impeded B-cell differentiation, while activation of D1-like receptor signals could promote B cell differentiation. Further RNA-seq confirmed that PTGS2, a gene related to B-cell differentiation, was up-regulated once the D1-like receptor signals were activated, while BMP6 and IL-24 were up-regulated once the D1-like receptor signals were inhibited. Conclusion D1-like receptors probably promote B-cell differentiation through the PTGS2/PRDM1 pathway. Systemic lupus erythematosus (dpeaa)DE-He213 Dopamine receptor (dpeaa)DE-He213 D1-like receptor (dpeaa)DE-He213 B cell (dpeaa)DE-He213 Therapeutic target (dpeaa)DE-He213 Wu, Fengxi verfasserin aut He, Zhenghao verfasserin aut Tan, Fen verfasserin aut Hu, Haoran verfasserin aut Zou, Chun verfasserin aut Yi, Ping verfasserin aut liu, Wenen verfasserin aut Yang, Ming verfasserin aut Enthalten in Cell communication and signaling BioMed Central, 2003 22(2024), 1 vom: 17. Okt. (DE-627)37375275X (DE-600)2126315-2 1478-811X nnns volume:22 year:2024 number:1 day:17 month:10 https://dx.doi.org/10.1186/s12964-024-01885-3 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 42.15 VZ AR 22 2024 1 17 10
allfieldsGer	10.1186/s12964-024-01885-3 doi (DE-627)SPR057846723 (SPR)s12964-024-01885-3-e DE-627 ger DE-627 rakwb eng 610 570 VZ 12 ssgn 42.15 bkl Xiang, Zhongyuan verfasserin aut D1-like dopamine receptors promote B-cell differentiation in systemic lupus erythematosus 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2024 Background Systemic lupus erythematosus (SLE) is an autoimmune disease that currently cannot be completely cured with a great health burden. Since the production of autoantibodies plays a key role in the pathogenesis of SLE, discovering the underlying immunoregulation mechanism of B cells will be helpful for developing promising immunotherapy for SLE. In recent studies, dopamine receptors (DRDs), G protein-coupled receptors that include D1-like and D2-like subtypes, are expressed on B cells and participate in various physiological processes, involving immune responses. However, the regulatory effect of DRDs on B cells has not been determined. Methods This study explored the expression of DRDs on B-cell subsets from SLE patients and healthy individuals. The effects of D1-like receptor on B-cell activation and differentiation were further explored using D1-like receptor agonists or antagonists. RNA-seq and bioinformatics analyses were used to identify specific molecular mechanisms involved. Results The D1-like DRDs on B cells of SLE patients were highly expressed compared with those of healthy controls (HCs). D1-like receptor agonist treatment exacerbated lupus-like symptoms in pristane-induced lupus-like mice, while D1-like receptor antagonists alleviated the lupus-like phenotypes. Inhibition of D1-like receptor signals impeded B-cell differentiation, while activation of D1-like receptor signals could promote B cell differentiation. Further RNA-seq confirmed that PTGS2, a gene related to B-cell differentiation, was up-regulated once the D1-like receptor signals were activated, while BMP6 and IL-24 were up-regulated once the D1-like receptor signals were inhibited. Conclusion D1-like receptors probably promote B-cell differentiation through the PTGS2/PRDM1 pathway. Systemic lupus erythematosus (dpeaa)DE-He213 Dopamine receptor (dpeaa)DE-He213 D1-like receptor (dpeaa)DE-He213 B cell (dpeaa)DE-He213 Therapeutic target (dpeaa)DE-He213 Wu, Fengxi verfasserin aut He, Zhenghao verfasserin aut Tan, Fen verfasserin aut Hu, Haoran verfasserin aut Zou, Chun verfasserin aut Yi, Ping verfasserin aut liu, Wenen verfasserin aut Yang, Ming verfasserin aut Enthalten in Cell communication and signaling BioMed Central, 2003 22(2024), 1 vom: 17. Okt. (DE-627)37375275X (DE-600)2126315-2 1478-811X nnns volume:22 year:2024 number:1 day:17 month:10 https://dx.doi.org/10.1186/s12964-024-01885-3 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 42.15 VZ AR 22 2024 1 17 10
allfieldsSound	10.1186/s12964-024-01885-3 doi (DE-627)SPR057846723 (SPR)s12964-024-01885-3-e DE-627 ger DE-627 rakwb eng 610 570 VZ 12 ssgn 42.15 bkl Xiang, Zhongyuan verfasserin aut D1-like dopamine receptors promote B-cell differentiation in systemic lupus erythematosus 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2024 Background Systemic lupus erythematosus (SLE) is an autoimmune disease that currently cannot be completely cured with a great health burden. Since the production of autoantibodies plays a key role in the pathogenesis of SLE, discovering the underlying immunoregulation mechanism of B cells will be helpful for developing promising immunotherapy for SLE. In recent studies, dopamine receptors (DRDs), G protein-coupled receptors that include D1-like and D2-like subtypes, are expressed on B cells and participate in various physiological processes, involving immune responses. However, the regulatory effect of DRDs on B cells has not been determined. Methods This study explored the expression of DRDs on B-cell subsets from SLE patients and healthy individuals. The effects of D1-like receptor on B-cell activation and differentiation were further explored using D1-like receptor agonists or antagonists. RNA-seq and bioinformatics analyses were used to identify specific molecular mechanisms involved. Results The D1-like DRDs on B cells of SLE patients were highly expressed compared with those of healthy controls (HCs). D1-like receptor agonist treatment exacerbated lupus-like symptoms in pristane-induced lupus-like mice, while D1-like receptor antagonists alleviated the lupus-like phenotypes. Inhibition of D1-like receptor signals impeded B-cell differentiation, while activation of D1-like receptor signals could promote B cell differentiation. Further RNA-seq confirmed that PTGS2, a gene related to B-cell differentiation, was up-regulated once the D1-like receptor signals were activated, while BMP6 and IL-24 were up-regulated once the D1-like receptor signals were inhibited. Conclusion D1-like receptors probably promote B-cell differentiation through the PTGS2/PRDM1 pathway. Systemic lupus erythematosus (dpeaa)DE-He213 Dopamine receptor (dpeaa)DE-He213 D1-like receptor (dpeaa)DE-He213 B cell (dpeaa)DE-He213 Therapeutic target (dpeaa)DE-He213 Wu, Fengxi verfasserin aut He, Zhenghao verfasserin aut Tan, Fen verfasserin aut Hu, Haoran verfasserin aut Zou, Chun verfasserin aut Yi, Ping verfasserin aut liu, Wenen verfasserin aut Yang, Ming verfasserin aut Enthalten in Cell communication and signaling BioMed Central, 2003 22(2024), 1 vom: 17. Okt. (DE-627)37375275X (DE-600)2126315-2 1478-811X nnns volume:22 year:2024 number:1 day:17 month:10 https://dx.doi.org/10.1186/s12964-024-01885-3 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 42.15 VZ AR 22 2024 1 17 10
language	English
source	Enthalten in Cell communication and signaling 22(2024), 1 vom: 17. Okt. volume:22 year:2024 number:1 day:17 month:10
sourceStr	Enthalten in Cell communication and signaling 22(2024), 1 vom: 17. Okt. volume:22 year:2024 number:1 day:17 month:10
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Systemic lupus erythematosus Dopamine receptor D1-like receptor B cell Therapeutic target
dewey-raw	610
isfreeaccess_bool	true
container_title	Cell communication and signaling
authorswithroles_txt_mv	Xiang, Zhongyuan @@aut@@ Wu, Fengxi @@aut@@ He, Zhenghao @@aut@@ Tan, Fen @@aut@@ Hu, Haoran @@aut@@ Zou, Chun @@aut@@ Yi, Ping @@aut@@ liu, Wenen @@aut@@ Yang, Ming @@aut@@
publishDateDaySort_date	2024-10-17T00:00:00Z
hierarchy_top_id	37375275X
dewey-sort	3610
id	SPR057846723
language_de	englisch
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Since the production of autoantibodies plays a key role in the pathogenesis of SLE, discovering the underlying immunoregulation mechanism of B cells will be helpful for developing promising immunotherapy for SLE. In recent studies, dopamine receptors (DRDs), G protein-coupled receptors that include D1-like and D2-like subtypes, are expressed on B cells and participate in various physiological processes, involving immune responses. However, the regulatory effect of DRDs on B cells has not been determined. Methods This study explored the expression of DRDs on B-cell subsets from SLE patients and healthy individuals. The effects of D1-like receptor on B-cell activation and differentiation were further explored using D1-like receptor agonists or antagonists. RNA-seq and bioinformatics analyses were used to identify specific molecular mechanisms involved. Results The D1-like DRDs on B cells of SLE patients were highly expressed compared with those of healthy controls (HCs). D1-like receptor agonist treatment exacerbated lupus-like symptoms in pristane-induced lupus-like mice, while D1-like receptor antagonists alleviated the lupus-like phenotypes. Inhibition of D1-like receptor signals impeded B-cell differentiation, while activation of D1-like receptor signals could promote B cell differentiation. Further RNA-seq confirmed that PTGS2, a gene related to B-cell differentiation, was up-regulated once the D1-like receptor signals were activated, while BMP6 and IL-24 were up-regulated once the D1-like receptor signals were inhibited. 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author	Xiang, Zhongyuan
spellingShingle	Xiang, Zhongyuan ddc 610 ssgn 12 bkl 42.15 misc Systemic lupus erythematosus misc Dopamine receptor misc D1-like receptor misc B cell misc Therapeutic target D1-like dopamine receptors promote B-cell differentiation in systemic lupus erythematosus
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topic_title	610 570 VZ 12 ssgn 42.15 bkl D1-like dopamine receptors promote B-cell differentiation in systemic lupus erythematosus Systemic lupus erythematosus (dpeaa)DE-He213 Dopamine receptor (dpeaa)DE-He213 D1-like receptor (dpeaa)DE-He213 B cell (dpeaa)DE-He213 Therapeutic target (dpeaa)DE-He213
topic	ddc 610 ssgn 12 bkl 42.15 misc Systemic lupus erythematosus misc Dopamine receptor misc D1-like receptor misc B cell misc Therapeutic target
topic_unstemmed	ddc 610 ssgn 12 bkl 42.15 misc Systemic lupus erythematosus misc Dopamine receptor misc D1-like receptor misc B cell misc Therapeutic target
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title	D1-like dopamine receptors promote B-cell differentiation in systemic lupus erythematosus
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title_full	D1-like dopamine receptors promote B-cell differentiation in systemic lupus erythematosus
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author_browse	Xiang, Zhongyuan Wu, Fengxi He, Zhenghao Tan, Fen Hu, Haoran Zou, Chun Yi, Ping liu, Wenen Yang, Ming
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title_sort	d1-like dopamine receptors promote b-cell differentiation in systemic lupus erythematosus
title_auth	D1-like dopamine receptors promote B-cell differentiation in systemic lupus erythematosus
abstract	Background Systemic lupus erythematosus (SLE) is an autoimmune disease that currently cannot be completely cured with a great health burden. Since the production of autoantibodies plays a key role in the pathogenesis of SLE, discovering the underlying immunoregulation mechanism of B cells will be helpful for developing promising immunotherapy for SLE. In recent studies, dopamine receptors (DRDs), G protein-coupled receptors that include D1-like and D2-like subtypes, are expressed on B cells and participate in various physiological processes, involving immune responses. However, the regulatory effect of DRDs on B cells has not been determined. Methods This study explored the expression of DRDs on B-cell subsets from SLE patients and healthy individuals. The effects of D1-like receptor on B-cell activation and differentiation were further explored using D1-like receptor agonists or antagonists. RNA-seq and bioinformatics analyses were used to identify specific molecular mechanisms involved. Results The D1-like DRDs on B cells of SLE patients were highly expressed compared with those of healthy controls (HCs). D1-like receptor agonist treatment exacerbated lupus-like symptoms in pristane-induced lupus-like mice, while D1-like receptor antagonists alleviated the lupus-like phenotypes. Inhibition of D1-like receptor signals impeded B-cell differentiation, while activation of D1-like receptor signals could promote B cell differentiation. Further RNA-seq confirmed that PTGS2, a gene related to B-cell differentiation, was up-regulated once the D1-like receptor signals were activated, while BMP6 and IL-24 were up-regulated once the D1-like receptor signals were inhibited. Conclusion D1-like receptors probably promote B-cell differentiation through the PTGS2/PRDM1 pathway. © The Author(s) 2024
abstractGer	Background Systemic lupus erythematosus (SLE) is an autoimmune disease that currently cannot be completely cured with a great health burden. Since the production of autoantibodies plays a key role in the pathogenesis of SLE, discovering the underlying immunoregulation mechanism of B cells will be helpful for developing promising immunotherapy for SLE. In recent studies, dopamine receptors (DRDs), G protein-coupled receptors that include D1-like and D2-like subtypes, are expressed on B cells and participate in various physiological processes, involving immune responses. However, the regulatory effect of DRDs on B cells has not been determined. Methods This study explored the expression of DRDs on B-cell subsets from SLE patients and healthy individuals. The effects of D1-like receptor on B-cell activation and differentiation were further explored using D1-like receptor agonists or antagonists. RNA-seq and bioinformatics analyses were used to identify specific molecular mechanisms involved. Results The D1-like DRDs on B cells of SLE patients were highly expressed compared with those of healthy controls (HCs). D1-like receptor agonist treatment exacerbated lupus-like symptoms in pristane-induced lupus-like mice, while D1-like receptor antagonists alleviated the lupus-like phenotypes. Inhibition of D1-like receptor signals impeded B-cell differentiation, while activation of D1-like receptor signals could promote B cell differentiation. Further RNA-seq confirmed that PTGS2, a gene related to B-cell differentiation, was up-regulated once the D1-like receptor signals were activated, while BMP6 and IL-24 were up-regulated once the D1-like receptor signals were inhibited. Conclusion D1-like receptors probably promote B-cell differentiation through the PTGS2/PRDM1 pathway. © The Author(s) 2024
abstract_unstemmed	Background Systemic lupus erythematosus (SLE) is an autoimmune disease that currently cannot be completely cured with a great health burden. Since the production of autoantibodies plays a key role in the pathogenesis of SLE, discovering the underlying immunoregulation mechanism of B cells will be helpful for developing promising immunotherapy for SLE. In recent studies, dopamine receptors (DRDs), G protein-coupled receptors that include D1-like and D2-like subtypes, are expressed on B cells and participate in various physiological processes, involving immune responses. However, the regulatory effect of DRDs on B cells has not been determined. Methods This study explored the expression of DRDs on B-cell subsets from SLE patients and healthy individuals. The effects of D1-like receptor on B-cell activation and differentiation were further explored using D1-like receptor agonists or antagonists. RNA-seq and bioinformatics analyses were used to identify specific molecular mechanisms involved. Results The D1-like DRDs on B cells of SLE patients were highly expressed compared with those of healthy controls (HCs). D1-like receptor agonist treatment exacerbated lupus-like symptoms in pristane-induced lupus-like mice, while D1-like receptor antagonists alleviated the lupus-like phenotypes. Inhibition of D1-like receptor signals impeded B-cell differentiation, while activation of D1-like receptor signals could promote B cell differentiation. Further RNA-seq confirmed that PTGS2, a gene related to B-cell differentiation, was up-regulated once the D1-like receptor signals were activated, while BMP6 and IL-24 were up-regulated once the D1-like receptor signals were inhibited. Conclusion D1-like receptors probably promote B-cell differentiation through the PTGS2/PRDM1 pathway. © The Author(s) 2024
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title_short	D1-like dopamine receptors promote B-cell differentiation in systemic lupus erythematosus
url	https://dx.doi.org/10.1186/s12964-024-01885-3
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author2	Wu, Fengxi He, Zhenghao Tan, Fen Hu, Haoran Zou, Chun Yi, Ping liu, Wenen Yang, Ming
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