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J Neuroimmunol. 2018 Dec 15;325:43-53. doi: 10.1016/j.jneuroim.2018.10.010. Epub 2018 Oct 23.

The TRPC6 intronic polymorphism, associated with the risk of neurological disorders in systemic lupus erythematous, influences immune cell function.

Author information

1
Unit of Immunology, Rheumatology, Allergy and Rare Diseases, IRCCS San Raffaele Hospital & Scientific Institute, Milan, Italy; Università Vita-Salute San Raffaele, Milan, Italy.
2
Università Vita-Salute San Raffaele, Milan, Italy.
3
Unit of Immunology, Rheumatology, Allergy and Rare Diseases, IRCCS San Raffaele Hospital & Scientific Institute, Milan, Italy.
4
Unit of Nephrology, IRCCS San Raffaele Hospital & Scientific Institute, Milan, Italy.
5
Unit of Immunology, Rheumatology, Allergy and Rare Diseases, IRCCS San Raffaele Hospital & Scientific Institute, Milan, Italy; Division of Immunology, Transplantation and Infectious Disease, San Raffaele Hospital & Scientific Institute Milan, Italy; Università Vita-Salute San Raffaele, Milan, Italy.
6
Division of Immunology, Transplantation and Infectious Disease, San Raffaele Hospital & Scientific Institute Milan, Italy. Electronic address: sciorati.clara@hsr.it.

Abstract

Patients with systemic lupus erythematosus (SLE) carrying a TT genotype for the rs7925662 single nucleotide polymorphism (SNP) in the transient receptor potential canonical channel 6 (TRPC6) gene are more likely to develop neuropsychiatric manifestations (NPSLE). We functionally characterised the effects of TRPC6 on peripheral blood mononuclear cells from 18 patients with SLE and 8 healthy controls with a known genotype. TRPC6 influenced calcium currents, apoptosis rates and cytokine secretion in a disease- and genotype-dependent manner. Cells from TT patients with NPSLE were more dependent on TRPC6 for the generation of calcium currents.

KEYWORDS:

Apoptosis; Calcium; Cytokines; Genetics; Neuropsychiatric; Systemic lupus erythematous; TRPC6

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