Publications

Publications 2019 – Partner 1

Basophil involvement in lupus nephritis: a basis for innovation in daily care. Icon for Silverchair Information Systems Related Articles

Basophil involvement in lupus nephritis: a basis for innovation in daily care.

Nephrol Dial Transplant. 2019 May 01;34(5):750-756

Authors: Charles N, Chemouny JM, Daugas E

Abstract
Lupus nephritis (LN) affects a large proportion of patients with systemic lupus erythematosus (SLE). LN can lead to end-stage renal disease depending on when it is diagnosed and on the adequacy of the treatment administered to the patient based on the class of LN. Determination of the class and activity of LN is only possible by histological analysis of kidney biopsies. In this context, the development of non-invasive early diagnostic tools for determining the class of LN and biomarkers predicting the response to treatment would greatly benefit patients with SLE. Basophils, which are one of the rarest types of circulating leucocytes, are well-established effectors of allergic and parasitic diseases. Recent advances in the understanding of the immune regulatory role of basophils in several auto immune conditions, including SLE and LN, have demonstrated their involvement in the amplification of auto-antibody production and LN pathogenesis in both human SLE and lupus-like mouse models. The present review summarizes the currently available literature describing dysregulation of basophil counts, basophil activation status and basophil activating factors in patients with SLE and the involvement of basophils in the pathogenesis of SLE. We also discuss the potential utility of these biological and immunological parameters as diagnostic and prognostic biomarkers, used alone or in combination with other known SLE and LN activity biomarkers. Finally, considering basophils as contributors to the disease, they may also constitute a future treatment target for the management of SLE and LN.

PMID: 31009949 [PubMed - in process]

TLR4 Receptor Induces 2-AG-Dependent Tolerance to Lipopolysaccharide and Trafficking of CB2 Receptor in Mast Cells. Icon for HighWire Related Articles

TLR4 Receptor Induces 2-AG-Dependent Tolerance to Lipopolysaccharide and Trafficking of CB2 Receptor in Mast Cells.

J Immunol. 2019 Apr 15;202(8):2360-2371

Authors: Espinosa-Riquer ZP, Ibarra-Sánchez A, Vibhushan S, Bratti M, Charles N, Blank U, Rodríguez-Manzo G, González-Espinosa C

Abstract
Mast cells (MCs) contribute to the control of local inflammatory reactions and become hyporesponsive after prolonged TLR4 activation by bacterial LPS. The molecular mechanisms involved in endotoxin tolerance (ET) induction in MCs are not fully understood. In this study, we demonstrate that the endocannabinoid 2-arachidonoylglycerol (2-AG) and its receptor, cannabinoid receptor 2 (CB2), play a role in the establishment of ET in bone marrow-derived MCs from C57BL/6J mice. We found that CB2 antagonism prevented the development of ET and that bone marrow-derived MCs produce 2-AG in a TLR4-dependent fashion. Exogenous 2-AG induced ET similarly to LPS, blocking the phosphorylation of IKK and the p65 subunit of NF-κB and inducing the synthesis of molecular markers of ET. LPS caused CB2 receptor trafficking in Rab11-, Rab7-, and Lamp2-positive vesicles, indicating recycling and degradation of the receptor. 2-AG also prevented LPS-induced TNF secretion in vivo, in a MC-dependent model of endotoxemia, demonstrating that TLR4 engagement leads to 2-AG secretion, which contributes to the negative control of MCs activation. Our study uncovers a functional role for the endocannabinoid system in the inhibition of MC-dependent innate immune responses in vivo.

PMID: 30814309 [PubMed - in process]

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