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CD38 promotes pristane-induced chronic inflammation and increases susceptibility to experimental lupus by an apoptosis-driven and TRPM2-dependent mechanism

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CD38 promotes pristane-induced chronic inflammation and increases susceptibility to experimental lupus by an apoptosis-driven and TRPM2-dependent mechanism. / García-Rodríguez, Sonia; Rosal-Vela, Antonio; Botta, Davide; Cumba Garcia, Luz M; Zumaquero, Esther; Prados-Maniviesa, Verónica; Cerezo-Wallis, Daniela; Lo Buono, Nicola; Robles-Guirado, José-Ángel; Guerrero, Salvador; González-Paredes, Elena; Andrés-León, Eduardo; Corbí, Ángel; Mack, Matthias; Koch-Nolte, Friedrich; Merino, Ramón; Zubiaur, Mercedes; Lund, Frances E; Sancho, Jaime.

in: SCI REP-UK, Jahrgang 8, Nr. 1, 20.02.2018, S. 3357.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

García-Rodríguez, S, Rosal-Vela, A, Botta, D, Cumba Garcia, LM, Zumaquero, E, Prados-Maniviesa, V, Cerezo-Wallis, D, Lo Buono, N, Robles-Guirado, J-Á, Guerrero, S, González-Paredes, E, Andrés-León, E, Corbí, Á, Mack, M, Koch-Nolte, F, Merino, R, Zubiaur, M, Lund, FE & Sancho, J 2018, 'CD38 promotes pristane-induced chronic inflammation and increases susceptibility to experimental lupus by an apoptosis-driven and TRPM2-dependent mechanism', SCI REP-UK, Jg. 8, Nr. 1, S. 3357. https://doi.org/10.1038/s41598-018-21337-6

APA

García-Rodríguez, S., Rosal-Vela, A., Botta, D., Cumba Garcia, L. M., Zumaquero, E., Prados-Maniviesa, V., Cerezo-Wallis, D., Lo Buono, N., Robles-Guirado, J-Á., Guerrero, S., González-Paredes, E., Andrés-León, E., Corbí, Á., Mack, M., Koch-Nolte, F., Merino, R., Zubiaur, M., Lund, F. E., & Sancho, J. (2018). CD38 promotes pristane-induced chronic inflammation and increases susceptibility to experimental lupus by an apoptosis-driven and TRPM2-dependent mechanism. SCI REP-UK, 8(1), 3357. https://doi.org/10.1038/s41598-018-21337-6

Vancouver

García-Rodríguez S, Rosal-Vela A, Botta D, Cumba Garcia LM, Zumaquero E, Prados-Maniviesa V et al. CD38 promotes pristane-induced chronic inflammation and increases susceptibility to experimental lupus by an apoptosis-driven and TRPM2-dependent mechanism. SCI REP-UK. 2018 Feb 20;8(1):3357. https://doi.org/10.1038/s41598-018-21337-6

Bibtex

@article{a46fadf85cde499ca9a1fe1839d920a9,
title = "CD38 promotes pristane-induced chronic inflammation and increases susceptibility to experimental lupus by an apoptosis-driven and TRPM2-dependent mechanism",
abstract = "In this study, we investigated the role of CD38 in a pristane-induced murine model of lupus. CD38-deficient (Cd38-/-) but not ART2-deficient (Art2-/-) mice developed less severe lupus compared to wild type (WT) mice, and their protective phenotype consisted of (i) decreased IFN-I-stimulated gene expression, (ii) decreased numbers of peritoneal CCR2hiLy6Chi inflammatory monocytes, TNF-α-producing Ly6G+ neutrophils and Ly6Clo monocytes/macrophages, (iii) decreased production of anti-single-stranded DNA and anti-nRNP autoantibodies, and (iv) ameliorated glomerulonephritis. Cd38-/- pristane-elicited peritoneal exudate cells had defective CCL2 and TNF-α secretion following TLR7 stimulation. However, Tnf-α and Cxcl12 gene expression in Cd38-/- bone marrow (BM) cells was intact, suggesting a CD38-independent TLR7/TNF-α/CXCL12 axis in the BM. Chemotactic responses of Cd38-/- Ly6Chi monocytes and Ly6G+ neutrophils were not impaired. However, Cd38-/- Ly6Chi monocytes and Ly6Clo monocytes/macrophages had defective apoptosis-mediated cell death. Importantly, mice lacking the cation channel TRPM2 (Trpm2-/-) exhibited very similar protection, with decreased numbers of PECs, and apoptotic Ly6Chi monocytes and Ly6Clo monocytes/macrophages compared to WT mice. These findings reveal a new role for CD38 in promoting aberrant inflammation and lupus-like autoimmunity via an apoptosis-driven mechanism. Furthermore, given the implications of CD38 in the activation of TRPM2, our data suggest that CD38 modulation of pristane-induced apoptosis is TRPM2-dependent.",
keywords = "Journal Article",
author = "Sonia Garc{\'i}a-Rodr{\'i}guez and Antonio Rosal-Vela and Davide Botta and {Cumba Garcia}, {Luz M} and Esther Zumaquero and Ver{\'o}nica Prados-Maniviesa and Daniela Cerezo-Wallis and {Lo Buono}, Nicola and Jos{\'e}-{\'A}ngel Robles-Guirado and Salvador Guerrero and Elena Gonz{\'a}lez-Paredes and Eduardo Andr{\'e}s-Le{\'o}n and {\'A}ngel Corb{\'i} and Matthias Mack and Friedrich Koch-Nolte and Ram{\'o}n Merino and Mercedes Zubiaur and Lund, {Frances E} and Jaime Sancho",
year = "2018",
month = feb,
day = "20",
doi = "10.1038/s41598-018-21337-6",
language = "English",
volume = "8",
pages = "3357",
journal = "SCI REP-UK",
issn = "2045-2322",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - CD38 promotes pristane-induced chronic inflammation and increases susceptibility to experimental lupus by an apoptosis-driven and TRPM2-dependent mechanism

AU - García-Rodríguez, Sonia

AU - Rosal-Vela, Antonio

AU - Botta, Davide

AU - Cumba Garcia, Luz M

AU - Zumaquero, Esther

AU - Prados-Maniviesa, Verónica

AU - Cerezo-Wallis, Daniela

AU - Lo Buono, Nicola

AU - Robles-Guirado, José-Ángel

AU - Guerrero, Salvador

AU - González-Paredes, Elena

AU - Andrés-León, Eduardo

AU - Corbí, Ángel

AU - Mack, Matthias

AU - Koch-Nolte, Friedrich

AU - Merino, Ramón

AU - Zubiaur, Mercedes

AU - Lund, Frances E

AU - Sancho, Jaime

PY - 2018/2/20

Y1 - 2018/2/20

N2 - In this study, we investigated the role of CD38 in a pristane-induced murine model of lupus. CD38-deficient (Cd38-/-) but not ART2-deficient (Art2-/-) mice developed less severe lupus compared to wild type (WT) mice, and their protective phenotype consisted of (i) decreased IFN-I-stimulated gene expression, (ii) decreased numbers of peritoneal CCR2hiLy6Chi inflammatory monocytes, TNF-α-producing Ly6G+ neutrophils and Ly6Clo monocytes/macrophages, (iii) decreased production of anti-single-stranded DNA and anti-nRNP autoantibodies, and (iv) ameliorated glomerulonephritis. Cd38-/- pristane-elicited peritoneal exudate cells had defective CCL2 and TNF-α secretion following TLR7 stimulation. However, Tnf-α and Cxcl12 gene expression in Cd38-/- bone marrow (BM) cells was intact, suggesting a CD38-independent TLR7/TNF-α/CXCL12 axis in the BM. Chemotactic responses of Cd38-/- Ly6Chi monocytes and Ly6G+ neutrophils were not impaired. However, Cd38-/- Ly6Chi monocytes and Ly6Clo monocytes/macrophages had defective apoptosis-mediated cell death. Importantly, mice lacking the cation channel TRPM2 (Trpm2-/-) exhibited very similar protection, with decreased numbers of PECs, and apoptotic Ly6Chi monocytes and Ly6Clo monocytes/macrophages compared to WT mice. These findings reveal a new role for CD38 in promoting aberrant inflammation and lupus-like autoimmunity via an apoptosis-driven mechanism. Furthermore, given the implications of CD38 in the activation of TRPM2, our data suggest that CD38 modulation of pristane-induced apoptosis is TRPM2-dependent.

AB - In this study, we investigated the role of CD38 in a pristane-induced murine model of lupus. CD38-deficient (Cd38-/-) but not ART2-deficient (Art2-/-) mice developed less severe lupus compared to wild type (WT) mice, and their protective phenotype consisted of (i) decreased IFN-I-stimulated gene expression, (ii) decreased numbers of peritoneal CCR2hiLy6Chi inflammatory monocytes, TNF-α-producing Ly6G+ neutrophils and Ly6Clo monocytes/macrophages, (iii) decreased production of anti-single-stranded DNA and anti-nRNP autoantibodies, and (iv) ameliorated glomerulonephritis. Cd38-/- pristane-elicited peritoneal exudate cells had defective CCL2 and TNF-α secretion following TLR7 stimulation. However, Tnf-α and Cxcl12 gene expression in Cd38-/- bone marrow (BM) cells was intact, suggesting a CD38-independent TLR7/TNF-α/CXCL12 axis in the BM. Chemotactic responses of Cd38-/- Ly6Chi monocytes and Ly6G+ neutrophils were not impaired. However, Cd38-/- Ly6Chi monocytes and Ly6Clo monocytes/macrophages had defective apoptosis-mediated cell death. Importantly, mice lacking the cation channel TRPM2 (Trpm2-/-) exhibited very similar protection, with decreased numbers of PECs, and apoptotic Ly6Chi monocytes and Ly6Clo monocytes/macrophages compared to WT mice. These findings reveal a new role for CD38 in promoting aberrant inflammation and lupus-like autoimmunity via an apoptosis-driven mechanism. Furthermore, given the implications of CD38 in the activation of TRPM2, our data suggest that CD38 modulation of pristane-induced apoptosis is TRPM2-dependent.

KW - Journal Article

U2 - 10.1038/s41598-018-21337-6

DO - 10.1038/s41598-018-21337-6

M3 - SCORING: Journal article

C2 - 29463868

VL - 8

SP - 3357

JO - SCI REP-UK

JF - SCI REP-UK

SN - 2045-2322

IS - 1

ER -