Expression of JAK Proteins and Autophagy Markers in Sjögren’s Syndrome Patients

María-José Barrera^1,2, Sergio Aguilera³, Isabel Castro², Patricia Carvajal², Sergio González⁴, Claudio Molina¹, Ulises Urzua² and María-Julieta González², ¹Facultad de Odontología, Universidad San Sebastián, Santiago, Chile, ²Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile, ³Reumatologia, Clinica Indisa, Santiago, Chile, ⁴Facultad de Odontología, Universidad Mayor, Santiago, Chile

Meeting: 2018 ACR/ARHP Annual Meeting

Keywords: autophagy, inflammation and salivary hypofunction, Janus kinase (JAK), Sjogren's syndrome

Session Information

Date: Monday, October 22, 2018

Session Title: Sjögren's Syndrome – Basic and Clinical Science Poster

Session Type: ACR Poster Session B

Session Time: 9:00AM-11:00AM

Background/Purpose:

Sjögren’s syndrome (SS) is an autoimmune epitheliitis that mainly affects the salivary and lachrymal glands. The glandular hypofunction has been associated to loss of epithelium by apoptosis. However, several lines of evidence indicate the existence of survival mechanisms that counteract the apoptosis, one of them being the autophagy. This mechanism is involved in decreasing inflammation by selectively removing proteins related to Toll-like receptors and inflammasomes, among other pathways. A previous study on SS showed increased autophagy in T lymphocytes of salivary glands, but the glandular epithelium was not evaluated. Interestingly, IL-6 implicated in SS pathogenesis mediates its response activating the JAK-STAT signaling pathway. In macrophages and other cellular types, activation of the JAK-STAT pathway inhibits autophagy. Studies in SS have shown increased expression of STATs, however, expression of JAK proteins has not been evaluated. The aim of this study was to evaluate the expression of JAKs proteins and autophagy markers in labial salivary glands from SS-patients.

Methods:

In labial salivary glands of 11 SS patients and 10 control subjects, mRNA levels of JAK1, JAK2, mTOR and ATG5 were measured by qPCR.

Results:

A significant decrease of JAK1 mRNA levels (p=0.0068), as well as decreased mRNA levels of genes that participate in autophagy such as mTOR and ATG5 (p=0.0074 and p=0.02, respectively) were observed in labial salivary glands of SS-patients.

Conclusion:

Low JAK1 mRNA levels in SS-patients suggest a downregulation mechanism in response to previously reported hyperactivation of JAK-STAT signaling pathway in SS patients. On the other hand, decreased mRNA levels of autophagy markers, such as ATG5 and mTOR, could indicate an attenuation of this pro-inflammatory mechanism in SS.

Funding: FONDECYT Postdoctoral Grant 3170023 (MJB, SA) and FONDECYT 1160015, (MJG, SA, CM, SG, IC).

Disclosure: M. J. Barrera, None; S. Aguilera, None; I. Castro, None; P. Carvajal, None; S. González, None; C. Molina, None; U. Urzua, None; M. J. González, None.

To cite this abstract in AMA style:

Barrera MJ, Aguilera S, Castro I, Carvajal P, González S, Molina C, Urzua U, González MJ. Expression of JAK Proteins and Autophagy Markers in Sjögren’s Syndrome Patients [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 10). https://acrabstracts.org/abstract/expression-of-jak-proteins-and-autophagy-markers-in-sjogrens-syndrome-patients/. Accessed May 30, 2020.

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