scholarly journals Type I interferons in Sjögren's syndrome

2013 ◽  
Vol 12 (5) ◽  
pp. 558-566 ◽  
Author(s):  
Yihong Yao ◽  
Zheng Liu ◽  
Bahija Jallal ◽  
Nan Shen ◽  
Lars Rönnblom
Keyword(s):  
Sjögren’S Syndrome ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Type I Interferons ◽  
Type I ◽  
Sjögren‘S Syndrome

scholarly journals The Transcriptomic Profile of Monocytes from Patients With Sjögren’s Syndrome Is Associated With Inflammatory Parameters and Is Mimicked by Circulating Mediators

2021 ◽  
Vol 12 ◽  
Author(s):  
Ana P. Lopes ◽  
Cornelis P. J. Bekker ◽  
Maarten R. Hillen ◽  
Sofie L. M. Blokland ◽  
Anneline C. Hinrichs ◽  
...  
Keyword(s):  
B Cell ◽  
Sjögren’S Syndrome ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Type I Interferons ◽  
Type I ◽  
Healthy Controls ◽  
Hub Genes ◽  
Sjögren‘S Syndrome

Primary Sjögren’s syndrome (pSS) is a systemic autoimmune disease characterized by infiltration of the exocrine glands and prominent B cell hyperactivity. Considering the key role of monocytes in promoting B cell hyperactivity, we performed RNA-sequencing analysis of CD14+ monocytes from patients with pSS, non-Sjögren’s sicca (nSS), and healthy controls (HC). We demonstrated that the transcriptomic profile of pSS patients is enriched in intermediate and non-classical monocyte profiles, and confirmed the increased frequency of non-classical monocytes in pSS patients by flow-cytometry analysis. Weighted gene co-expression network analysis identified four molecular signatures in monocytes from pSS patients, functionally annotated for processes related with translation, IFN-signaling, and toll-like receptor signaling. Systemic and local inflammatory features significantly correlated with the expression of these signatures. Furthermore, genes highly associated with clinical features in pSS were identified as hub-genes for each signature. Unsupervised hierarchical cluster analysis of the hub-genes identified four clusters of nSS and pSS patients, each with distinct inflammatory and transcriptomic profiles. One cluster showed a significantly higher percentage of pSS patients with higher prevalence of anti-SSA autoantibodies, interferon-score, and erythrocyte sedimentation rate compared to the other clusters. Finally, we showed that the identified transcriptomic differences in pSS monocytes were induced in monocytes of healthy controls by exposure to serum of pSS patients. Representative hub-genes of all four signatures were partially inhibited by interferon-α/β receptor blockade, indicating that the circulating inflammatory mediators, including type I interferons have a significant contribution to the altered transcriptional profile of pSS-monocytes. Our study suggests that targeting key circulating inflammatory mediators, such as type I interferons, could offer new insights into the important pathways and mechanisms driving pSS, and holds promise for halting immunopathology in Sjögren’s Syndrome.

scholarly journals HTLV-I Associated uveitis, myelopathy, rheumatoid arthritis and Sjögren's syndrome

1995 ◽  
Vol 53 (4) ◽  
pp. 777-781 ◽  
Author(s):  
Sônia Regina A. A. Pinheiro ◽  
Marco Aurélio Lana-Peixoto ◽  
Anna B. Carneiro Proietti ◽  
Fernando Oréfice ◽  
Maria V. Lima-Martins ◽  
...  
Keyword(s):  
Sjögren’S Syndrome ◽  
Sjögren's Syndrome ◽  
Spastic Paraparesis ◽  
Clinical Manifestations ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Lower Limbs ◽  
Type I ◽  
Human T Cell ◽  
Sjögren‘S Syndrome

A 62 year-old white female presented with a 10-year-history of slowly progressive spastic paraparesis, pain and dysesthesia in the lower limbs and sphincter disturbance. A few years after the onset of the neurologic symptoms she developped migratory arthritis with swelling of the knees and pain on palpation of knees and fingers, dry eyes, mouth and skin. Two months before admission she presented bilateral nongranulomatous anterior uveitis. Examination revealed spastic paraparesis with bilateral Babinski sign, a decreased sensation level below L3, decreased vibration sense in the lower extremities, and a postural tremor of the upper limbs. Laboratory work-up disclosed HTLV-I positive tests in the blood and cerebrospinal fluid (CSF), and a mild pleocytosis in the CSF with a normal protein content. Nerve conduction velocity studies were normal. The present case shows the association of uveitis, arthritis and Sjögren's syndrome in a patient with tropical spastic paraparesis / human T-cell lymphotropic virus type I (HTLV-I) associated myelopathy (TSP/HAM), and illustrates the wide spectrum of clinical manifestations which may accompany this infection with this virus.

Relationship between Sjögren's syndrome and human T-lymphotropic virus type I infection: Follow-up study of 83 patients

2000 ◽  
Vol 135 (2) ◽  
pp. 139-144 ◽  
Author(s):  
Hideki Nakamura ◽  
Atsushi Kawakami ◽  
Masahiro Tominaga ◽  
Ayumi Hida ◽  
Satoshi Yamasaki ◽  
...  
Keyword(s):  
Sjögren’S Syndrome ◽  
Virus Type ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Type I ◽  
T Lymphotropic Virus ◽  
Follow Up Study ◽  
Sjögren‘S Syndrome

Renal tubular acidosis as a clinical presentation of Sjögren's syndrome: case report

2019 ◽  
pp. 26-28
Author(s):  
D. Fernández Ávila ◽  
A. Vargas Caselles ◽  
O. Diz
Keyword(s):  
Sjögren’S Syndrome ◽  
Renal Tubular Acidosis ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Type I ◽  
Ammonium Excretion ◽  
Patient Reported ◽  
Renal Tubular ◽  
Sjögren‘S Syndrome

We present the clinical case of a woman in the fifth decade of life, argentina, who went to the Internal Medicine emergency room of a third level hospital for symptoms of myalgia and paresis in all four extremities, acute onset, progressive, with difficulty for the mobilization of members superior, standing and walking. Severe hypokalemia, metabolic acidosis, alkaline urinary pH, positive urinary anion GAP (ammonium excretion), hypocitraturia and hypercalciuria were diagnosed. Renal Tubular Acidosis (RTA) type I was diagnosed; acute renal failure was also noted, which corrected with the treatment and elevated creatine kinase (CK). In the anamnesis, the patient reported dry syndrome associated with arthralgias of years of evolution, so that complementary studies were carried out that supported the diagnosis of Sjögren’s Syndrome (SS).

scholarly journals Sjogren’s Syndrome and TAM Receptors: A Possible Contribution to Disease Onset

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Richard Witas ◽  
Ammon B. Peck ◽  
Julian L. Ambrus ◽  
Cuong Q. Nguyen
Keyword(s):  
Autoimmune Disease ◽  
Sjögren’S Syndrome ◽  
Lupus Erythematosus ◽  
Sjögren's Syndrome ◽  
Disease Onset ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Type I ◽  
Apoptotic Cells ◽  
Sjögren‘S Syndrome

Sjogren’s syndrome (SS) is a chronic, progressive autoimmune disease featuring both organ-specific and systemic manifestations, the most frequent being dry mouth and dry eyes resulting from lymphocytic infiltration into the salivary and lacrimal glands. Like the related autoimmune disease systemic lupus erythematosus (SLE), SS patients and mouse models display accumulation of apoptotic cells and a Type I interferon (IFN) signature. Receptor tyrosine kinases (RTKs) of the Tyro3, Axl, and Mer (TAM) family are present on the surface of macrophages and dendritic cells and participate in phagocytosis of apoptotic cells (efferocytosis) and inhibition of Type I IFN signaling. This review examines the relationship between TAM receptor dysfunction and SS and explores the potential contributions of TAM defects on macrophages to SS development.

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