Sjögren's syndrome in MRL/l and MRL/n mice

Hoffman, Robert W.; Alspaugh, Margaret A.; Waggie, Kim; Durham, J.; Walker, Sara E.

doi:10.1002/art.1780270206

Cited by 139 publications

(104 citation statements)

References 24 publications

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“…The effect on saliva secretion continued even with chronically administered Cevimeline, and these effects continued for at least 4 weeks after Cevimeline discontinuation. The MRL/l mice (SS mice) used in this study were those with autoimmune disorders that naturally develop symptoms of sialadenitis or angiitis, and exhibit lymphocytic infiltrate around the ducts and blood vessels due to aging [15][16][17][18].…”

Section: Discussionmentioning

confidence: 99%

“…AQP-5 was found to be mainly related to saliva secretion, whereas the localization of AQP-1, 3, 4 and 8 is thought to affect saliva composition. The relationship between the localization of AQP-5, using MRL/MpJ-Tnfrsf6 lpr /Crlj (MRL/l) mice [15][16][17][18] that naturally develop symptoms of sialadenitis or angiitis was also shown. We conducted a histological study on the inflammatory changes in the salivary gland tissues of the salivary glands of 4 groups: a group of SS mice not administered Cevimeline, a group of SS mice administrated Cevimeline, a group of SS mice chronically administered Cevimeline, a group that received but then discontinued Cevimeline, and a group of normal mice not administered Cevimeline.…”

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confidence: 95%

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An Immunohistochemistry-Based Study on Aquaporin (AQP)-1, 3, 4, 5 and 8 in the Parotid Glands, Submandibular Glands and Sublingual Glands of Sj^|^ouml;gren^|^rsquo;s Syndrome Mouse Models Chronically Administered Cevimeline

et al. 2013

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 95%

An Immunohistochemistry-Based Study on Aquaporin (AQP)-1, 3, 4, 5 and 8 in the Parotid Glands, Submandibular Glands and Sublingual Glands of Sj^|^ouml;gren^|^rsquo;s Syndrome Mouse Models Chronically Administered Cevimeline

et al. 2013

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“…Sialadenitis in MRL/lpr mice is histopathologically characterized initially by mononuclear cell infiltration into periductular regions, followed by the progressive destruction of ductules and parenchyma, resembling the features of SS (4,5).…”

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confidence: 99%

Antagonist of interferon‐inducible protein 10/CXCL10 ameliorates the progression of autoimmune sialadenitis in MRL/lpr mice

Hasegawa¹,

Inoue²,

Kohno³

et al. 2006

Arthritis & Rheumatism

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Objective. Mononuclear cell infiltration of the salivary glands is a major feature of Sjögren's syndrome (SS) and its animal model. Local generation of chemokines and the presence of chemokine receptors on the infiltrating cells may be involved in this process. We undertook the present study to investigate the expression of chemokines during the development of autoimmune sialadenitis in MRL/lpr mice and the therapeutic effect of chemokine antagonists on sialadenitis.Methods. NH 2 -terminal-truncated interferoninducible protein 10 (IP-10)/CXCL10 analogs were transfected into a nonmetastatic fibroblastoid cell line, MRL/N-1, and injected subcutaneously into MRL/lpr mice, and the effects on sialadenitis were monitored.Results. IP-10 analogs truncated by 5 or more amino acid residues from the N-terminal failed to induce chemotaxis and calcium influx by CXCR3-expressing cells. Of these, the most potent antagonist (AT) (IP-10-AT) was a molecule with methionine added after removal of the 5 N-terminal amino acid residues. Significantly increased expression of the Th1-associated chemokines IP-10, monokine induced by interferon-␥/ CXCL9, and interferon-inducible T cell chemoattractant/CXCL11 was induced in the ductal epithelium by interferon-␥ produced in the salivary glands, whereas expression of the Th2-associated chemokines thymus and activation-regulated chemokine (TARC)/ CCL17 and monocyte-derived chemokine/CCL22 was almost undetectable during sialadenitis. Inoculation of IP-10-AT into MRL/lpr mice during the early stage of sialadenitis significantly reduced periductal mononuclear cell infiltration and parenchymal destruction compared with these features in control and TARC-ATbearing mice. This was due to a significant reduction in infiltration of CXCR3؉ T cells, predominantly Th1 cells, resulting in decreased interferon-␥ production.Conclusion. We prepared a novel potent IP-10 antagonist and demonstrated its ability to ameliorate the progression of autoimmune sialadenitis. This agent may provide a new therapeutic approach to SS.

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“…Two of those models, the nonobese diabetic (NOD) mouse and the MRL/lpr mouse, are widely accepted (Hayashi et al, 1994;Hoffman et al, 1984;Humphreys-Beher, 1996). In both mouse strains, perivascular and periductal lymphocytic infiltrates in the salivary and lacrimal glands are histologic hallmarks of the disease.…”

mentioning

confidence: 99%

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?

Blokland

Helden-Meeuwsen

Wierenga‐Wolf

et al. 2000

Laboratory Investigation

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SUMMARY: Sjö gren's syndrome is an autoimmune disease that primarily affects the salivary and lacrimal glands. In these glands, focal lymphocytic infiltrates develop. Little is known about the initiation of this autoimmune disease. Antigen-presenting cells (APC) such as dendritic cells (DC) can play a role in the initiation of autoimmunity. To date, no data on the presence of DC in Sjö gren's syndrome are available. Several mouse strains, the nonobese diabetic (NOD) and the MRL/lpr mouse, can be used as models for Sjö gren's syndrome. We compared the development of sialoadenitis in the submandibular glands (SMG) of NOD and MRL/lpr mice with particular focus on the presence of APC. DC, macrophages, T cells, and B cells in the SMG were studied by means of immunohistochemistry, after which positively stained cells were quantified. NOD-severe combined immunodeficiency (SCID) mice were used to study the presence of APC in the SMG in the absence of lymphocytes. Before lymphocytic infiltration, increased numbers of DC were detected in the SMG of NOD mice compared with those numbers in control mice and MRL/lpr mice, which suggests that DC play a role in the initiation of sialoadenitis in NOD mice. In the SMG of NOD mice, lymphocytic infiltrates organized in time. In MRL/lpr mice, however, lymphocytic infiltrates were already organized at the time of appearance. This organization was lost over time. In conclusion, two types of sialoadenitis are described in two mouse models for Sjö gren's syndrome. Differences exist with regard to early events that may lead to the development of sialoadenitis and to the composition and organization of inflammatory infiltrates. It is possible that different types of sialoadenitis also exist in humans and that the pathogenetic process in both the early and late phases of the autoimmune reaction differs among patients. (Lab Invest 2000, 80:575-585).

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Sjögren's syndrome in MRL/l and MRL/n mice

Cited by 139 publications

References 24 publications

An Immunohistochemistry-Based Study on Aquaporin (AQP)-1, 3, 4, 5 and 8 in the Parotid Glands, Submandibular Glands and Sublingual Glands of Sj^|^ouml;gren^|^rsquo;s Syndrome Mouse Models Chronically Administered Cevimeline

An Immunohistochemistry-Based Study on Aquaporin (AQP)-1, 3, 4, 5 and 8 in the Parotid Glands, Submandibular Glands and Sublingual Glands of Sj^|^ouml;gren^|^rsquo;s Syndrome Mouse Models Chronically Administered Cevimeline

Antagonist of interferon‐inducible protein 10/CXCL10 ameliorates the progression of autoimmune sialadenitis in MRL/lpr mice

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?

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