Androgen-Induced Suppression of Autoimmune Disease in Lacrimal Glands of Mouse Models of Sjögren’s Syndrome

1994 ◽  
pp. 683-690 ◽  
Author(s):  
David A. Sullivan ◽  
Hiroko Ariga ◽  
Ana C. Vendramini ◽  
Flavio J. Rocha ◽  
Masafumi Ono ◽  
...  
Keyword(s):  
Autoimmune Disease ◽  
Sjögren’S Syndrome ◽  
Mouse Models ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Lacrimal Glands ◽  
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.

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 TLR7 Signaling Drives the Development of Sjögren’s Syndrome

2021 ◽  
Vol 12 ◽  
Author(s):  
Yawen Wang ◽  
Annie Roussel-Queval ◽  
Lionel Chasson ◽  
Noël Hanna Kazazian ◽  
Laetitia Marcadet ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Autoimmune Disease ◽  
Salivary Glands ◽  
Sjögren’S Syndrome ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Autoantibody Production ◽  
Deficient Mice ◽  
Sjögren‘S Syndrome

Sjögren’s syndrome (SS) is a chronic systemic autoimmune disease that affects predominately salivary and lacrimal glands. SS can occur alone or in combination with another autoimmune disease like systemic lupus erythematosus (SLE). Here we report that TLR7 signaling drives the development of SS since TLR8-deficient (TLR8ko) mice that develop lupus due to increased TLR7 signaling by dendritic cells, also develop an age-dependent secondary pathology similar to associated SS. The SS phenotype in TLR8ko mice is manifested by sialadenitis, increased anti-SSA and anti-SSB autoantibody production, immune complex deposition and increased cytokine production in salivary glands, as well as lung inflammation. Moreover, ectopic lymphoid structures characterized by B/T aggregates, formation of high endothelial venules and the presence of dendritic cells are formed in the salivary glands of TLR8ko mice. Interestingly, all these phenotypes are abrogated in double TLR7/8-deficient mice, suggesting that the SS phenotype in TLR8-deficient mice is TLR7-dependent. In addition, evaluation of TLR7 and inflammatory markers in the salivary glands of primary SS patients revealed significantly increased TLR7 expression levels compared to healthy individuals, that were positively correlated to TNF, LT-α, CXCL13 and CXCR5 expression. These findings establish an important role of TLR7 signaling for local and systemic SS disease manifestations, and inhibition of such will likely have therapeutic value.

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