sialadenitis/offita

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Agonist-induced 4-1BB activation prevents the development of Sjӧgren's syndrome-like sialadenitis in non-obese diabetic mice.

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Activation of costimulatory receptor 4-1BB enhances T helper 1 (Th1) and CD8 T cell responses in protective immunity, and prevents or attenuates several autoimmune diseases by increasing Treg numbers and suppressing Th17 or Th2 effector response. We undertook this study to elucidate the impact of

Detection of alterations in the levels of neuropeptides and salivary gland responses in the non-obese diabetic mouse model for autoimmune sialoadenitis.

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The salivary glands of non-obese diabetic (NOD) mice and BALB/c controls were evaluated for the stimulatory effects of the following neuropeptides; substance P (SP), vasoactive intestinal polypeptide (VIP), and neuropeptide Y (NPY). Injection of either of the three neuropeptides in combination with

[Study on total glucosides of peony preventing non-obese diabetic mice from sialoadenitis].

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OBJECTIVE To investigate the immunosuppressive effect of total glucosides of peony (TGP) on sialoadenitis in non-obese diabetic mice (NOD mice) and explore its possible mechanism. METHODS 27 female five-week-old NOD mice were randomly divided into three groups: TGP, hydroxychloroquine (HCQ) and

Defective signalling in salivary glands precedes the autoimmune response in the non-obese diabetic mouse model of sialadenitis.

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The spontaneous non-obese diabetic (NOD) mouse model of Sjögren's syndrome provides a valuable tool to study the onset and progression of both the autoimmune response and secretory dysfunction. Our purpose was to analyse the temporal decline of salivary secretion in NOD mice in relation to the

Decreased submandibular adiponectin is involved in the progression of autoimmune sialoadenitis in non-obese diabetic mice.

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OBJECTIVE To investigate a possible role of adiponectin in the pathogenesis of autoimmune sialoadenitis in non-obese diabetic (NOD) mouse model of Sjögren's syndrome. METHODS Expression of adiponectin and its receptors (AdipoR1/2) was detected by PCR, immunoblotting, or immunofluorescence. The level

Salivary-gland-protective regulatory T-cell dysfunction underlies female-specific sialadenitis in the non-obese diabetic mouse model of Sjögren syndrome.

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Immune cell-mediated destruction of salivary glands is a hallmark feature of Sjögren syndrome. Similar to the female predominance in humans, female non-obese diabetic (NOD) mice develop spontaneous salivary gland autoimmunity. However, in both humans and mice it is unclear what factors contribute to

Involvement of toll-like receptors in autoimmune sialoadenitis of the non-obese diabetic mouse.

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The aim of this study was to characterize the expression of Toll-like receptors (TLRs) during the development of sialoadenitis in the non-obese diabetic mouse. Submandibular glands were dissected from non-obese diabetic mice at 4, 8, 10, 12, and 16 weeks of age. The mRNA expression levels of TLR1,

Non-obese diabetic mice hemizygous at the T cell receptor alpha locus are susceptible to diabetes and sialitis.

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To test the hypothesis that T cells carrying two T cell receptor (TCR) alpha chains play a role in autoimmunity, we backcrossed the non-obese diabetic (NOD) strain with one carrying a TCR alpha gene disrupted by homologous recombination. Mice carrying one copy of the disrupted gene are incapable of

TACI-Fc gene therapy improves autoimmune sialadenitis but not salivary gland function in non-obese diabetic mice.

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OBJECTIVE Patients with Sjögren's syndrome (SS) show aberrant expression of the B cell-related mediators, B cell-activating factor (BAFF), and a proliferation-inducing ligand (APRIL) in serum and salivary glands (SGs). We studied the biological effect of neutralizing these cytokines by local gene

Analysis of T cell receptor Vbeta usage in the autoimmune sialadenitis of non-obese diabetic (NOD) mice.

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The NOD mouse develops spontaneous autoimmune sialadenitis besides a well characterized T cell-mediated autoimmune insulitis. We used reverse transcriptase-polymerase chain reaction (RT-PCR) to analyse the repertoire of T cell receptor (TCR) Vbeta chain genes expressed in the isolated infiltrating

Pathogenic role of endogenous TNF-α in the development of Sjögren's-like sialadenitis and secretory dysfunction in non-obese diabetic mice.

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Patients with Sjögren's syndrome (SS), an autoimmune disease primarily affecting exocrine glands, exhibit enhanced TNF-α expression in the saliva and salivary glands. However, the precise in vivo role of TNF-α during the initiation and development of SS is not clearly defined. The present study is

Non-depleting anti-CD4 antibody not only prevents onset but resolves sialadenitis in NOD mice.

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The non-obese diabetic (NOD) mouse spontaneously develops lymphocytic infiltrates in the salivary glands (sialadenitis) and provides an useful rodent model of human Sjogren's syndrome (SS). Non-depleting anti-CD4 antibodies have been shown to ameliorate Type 1 diabetes in NOD mice and also

The genetic control of sialadenitis versus arthritis in a NOD.QxB10.Q F2 cross.

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The non-obese diabetic (NOD) mouse spontaneously develops diabetes and sialadenitis. The sialadenitis is characterized by histopathological changes in salivary glands and functional deficit similar to Sjögren's syndrome. In humans, Sjögren's syndrome could be associated with other connective tissue

Protein kinase C expression in salivary gland acinar epithelial cells in non-obese diabetic mice, an experimental model for Sjögren's syndrome.

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We planned to investigate the expression of protein kinase C (PKC) isoforms in acinar epithelial cells of salivary glands in the non-obese diabetic (NOD) mouse to find out if they develop changes of the PKC system like those seen in the human counterpart, i.e. in Sjögren's syndrome. Parotid,

Adrenalitis in the non-obese diabetic mouse.

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The non-obese diabetic (NOD) mouse is a model of spontaneous type-1 diabetes used in the field of diabetes research. This study looked at the adrenal glands of NOD and control mice both indirectly in vivo for hormone secretion, and directly in vitro for histological examination. Adrenal glands were

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