Usefulness of mouse models to study the pathogenesis of Sjögren's syndrome

Oral Diseases ◽  
2007 ◽  
Vol 13 (4) ◽  
pp. 366-375 ◽  
Author(s):  
MS Soyfoo ◽  
S Steinfeld ◽  
C Delporte
Keyword(s):  
Sjögren’S Syndrome ◽  
Mouse Models ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Sjögren‘S Syndrome

Impact of Gender on Exocrine Gland Inflammation in Mouse Models of Sjögren's Syndrome

1999 ◽  
Vol 69 (4) ◽  
pp. 355-366 ◽  
Author(s):  
IKUKO TODA ◽  
BENJAMIN D SULLIVAN ◽  
EDUARDO M ROCHA ◽  
LILIA A DA SILVEIRA ◽  
L.ALEXANDRA WICKHAM ◽  
...  
Keyword(s):  
Sjögren’S Syndrome ◽  
Mouse Models ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Exocrine Gland ◽  
Sjögren‘S Syndrome

scholarly journals GABA Administration Ameliorates Sjogren’s Syndrome in Two Different Mouse Models

Biomedicines ◽  
2022 ◽  
Vol 10 (1) ◽  
pp. 129
Author(s):  
Min Song ◽  
Jide Tian ◽  
Blake Middleton ◽  
Cuong Q. Nguyen ◽  
Daniel L. Kaufman
Keyword(s):  
Sjögren’S Syndrome ◽  
Mouse Models ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Exocrine Function ◽  
Tear Production ◽  
Lymphocytic Infiltrates ◽  
Chronic Autoimmune Disease ◽  
Sjögren‘S Syndrome

Sjögren’s syndrome (SS) is a chronic autoimmune disease characterized by lymphocytic infiltrates in the salivary and lachrymal glands resulting in oral and ocular dryness. There are no clinically approved therapies to slow the progression of SS. Immune cells possess receptors for the neurotransmitter GABA (GABA-Rs) and their activation has immunoregulatory actions. We tested whether GABA administration has potential for amelioration of SS in NOD.B10-H2b and C57BL/6.NOD-Aec1Aec2 mice, two spontaneous SS models. Oral GABA treatment was initiated (1) after the development of sialadenitis but before the onset of overt symptoms, or (2) after the appearance of overt symptoms. When assessed weeks later, GABA-treated mice had greater saliva and tear production, as well as quicker times to salvia flow, in both SS mouse models. This was especially evident when GABA treatment was initiated after the onset of overt disease. This preservation of exocrine function was not accompanied by significant changes in the number or area of lymphocytic foci in the salivary or lachrymal glands of GABA-treated mice and we discuss the possible reasons for these observations. Given that GABA-treatment preserved saliva and tear production which are the most salient symptoms of SS and is safe for consumption, it may provide a new approach to help ameliorate SS.

scholarly journals Contributions of Major Cell Populations to Sjögren’s Syndrome

2020 ◽  
Vol 9 (9) ◽  
pp. 3057 ◽  
Author(s):  
Richard Witas ◽  
Shivai Gupta ◽  
Cuong Q. Nguyen
Keyword(s):  
B Cell ◽  
Sjögren’S Syndrome ◽  
Mouse Models ◽  
Immune Cells ◽  
Immune Cell ◽  
Sjögren's Syndrome ◽  
B Cell Lymphoma ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Sjögren‘S Syndrome

Sjögren’s syndrome (SS) is a female dominated autoimmune disease characterized by lymphocytic infiltration into salivary and lacrimal glands and subsequent exocrine glandular dysfunction. SS also may exhibit a broad array of extraglandular manifestations including an elevated incidence of non-Hodgkin’s B cell lymphoma. The etiology of SS remains poorly understood, yet progress has been made in identifying progressive stages of disease using preclinical mouse models. The roles played by immune cell subtypes within these stages of disease are becoming increasingly well understood, though significant gaps in knowledge still remain. There is evidence for distinct involvement from both innate and adaptive immune cells, where cells of the innate immune system establish a proinflammatory environment characterized by a type I interferon (IFN) signature that facilitates propagation of the disease by further activating T and B cell subsets to generate autoantibodies and participate in glandular destruction. This review will discuss the evidence for participation in disease pathogenesis by various classes of immune cells and glandular epithelial cells based upon data from both preclinical mouse models and human patients. Further examination of the contributions of glandular and immune cell subtypes to SS will be necessary to identify additional therapeutic targets that may lead to better management of the disease.

scholarly journals Recent Advances in Mouse Models of Sjögren's Syndrome

2020 ◽  
Vol 11 ◽  
Author(s):  
Yunzhen Gao ◽  
Yan Chen ◽  
Zhongjian Zhang ◽  
Xinhua Yu ◽  
Junfeng Zheng
Keyword(s):  
Sjögren’S Syndrome ◽  
Mouse Models ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Recent Advances ◽  
Sjögren‘S Syndrome

scholarly journals Two Different Types of Sialoadenitis in the NOD- and MRL/lpr Mouse Models for Sjögren’s Syndrome: A Differential Role for Dendritic Cells in the Initiation of Sialoadenitis?

2000 ◽  
Vol 80 (4) ◽  
pp. 575-585 ◽  
Author(s):  
Saskia C A van Blokland ◽  
Cornelia G van Helden-Meeuwsen ◽  
Annet F Wierenga-Wolf ◽  
Hemmo A Drexhage ◽  
Herbert Hooijkaas ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Sjögren’S Syndrome ◽  
Mouse Models ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Different Types ◽  
Sjögren‘S Syndrome

scholarly journals Current Concepts: Mouse Models of Sjögren's Syndrome

2011 ◽  
Vol 2011 ◽  
pp. 1-14 ◽  
Author(s):  
Tegan N. Lavoie ◽  
Byung Ha Lee ◽  
Cuong Q. Nguyen
Keyword(s):  
Autoimmune Disease ◽  
Sjögren’S Syndrome ◽  
Mouse Models ◽  
Lupus Erythematosus ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Unknown Etiology ◽  
Biliary Cirrhosis ◽  
Sjögren‘S Syndrome

Sjögren's syndrome (SjS) is a complex chronic autoimmune disease of unknown etiology which primarily targets the exocrine glands, resulting in eventual loss of secretory function. The disease can present as either primary SjS or secondary SjS, the latter of which occurs concomitantly with another autoimmune disease such as rheumatoid arthritis, systemic lupus erythematosus, scleroderma, or primary biliary cirrhosis. Current advancements in therapeutic prevention and treatment for SjS are impeded by lack of understanding in the pathophysiological and clinical progression of the disease. Development of appropriate mouse models for both primary and secondary SjS is needed in order to advance knowledge of this disease. This paper details important features, advantages, and pitfalls of current animal models of SjS, including spontaneous, transgenic, knockout, immunization, and transplantation chimera mouse models, and emphasizes the need for a better model in representing the human SjS phenotype.

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