"Facts and myths in Sjö gren's syndrome DJ Aframian et al auto-Abs were reported in pSjS (8 of 9 patients), but not in SLE (0 of 6) or healthy controls (0 of 12) (Winer et al, 2002), but this report could not be confirmed (Gordon et al, 2004). In a non-obese diabetic (NOD) mouse model of SjS, in which spontaneous lymphocytic infiltration of the lacrimal and salivary glands occurs, disruption of the ICA69 gene reduced sialadenitis or dacryoadenitis, while ICA69-specific T cells were identified in the lymph nodes of diseased NOD mice (Winer et al, 2002). "
[Show abstract][Hide abstract] ABSTRACT: Oral Diseases (2012) 19, 46–58
Sjögren’s syndrome (SjS) is one of the most common autoimmune rheumatic diseases, clinically characterized by xerostomia and keratoconjunctivitis sicca. We investigated the following controversial topics: (i) Do we have reliable ways of assessing saliva production? (ii) How important are the quantity and quality of saliva? (iii) Are only anti-SSA/Ro and anti-SSB/La relevant for the diagnosis of SjS? (iv) Are the American-European Consensus criteria (AECC) the best way to diagnose SjS? Results from literature searches suggested the following: (i) Despite the fact that numerous tests are available to assess salivation rates, direct comparisons among them are scarce with little evidence to suggest one best test. (ii) Recent developments highlight the importance of investigating the composition of saliva. However, more research is needed to standardize the methods of analysis and collection and refine the quality of the accumulating data. (iii) In addition to anti-Ro/La autoantibodies, anti α-fodrin IgA and anti-MR3 autoantibodies seem to be promising diagnostic markers of SjS, but more studies are warranted to test their sensitivity and specificity. (iv) AECC are classification, not diagnostic criteria. Moreover, recent innovations have not been incorporated into these criteria. Consequently, treatment directed to patients diagnosed using the AECC might exclude a significant proportion of patients with SjS.
"Disruption of the islet-cell autoantigen 69 kDa gene in NOD mice, a self-antigen associated with diabetes that is expressed not only in the pancreas but also in the exocrine glands, reduced SS-related histopathology and glandular hypofunction . A study investigating a large cohort of patients with SS could not, however, confirm a role or true frequency of islet-cell autoantigen 69 kDa autoimmunity in patients with SS . Studying the role of autoimmune regulator deficiency and central tolerance in the context of SS in NOD and Balb/c mice identified odorant binding protein 1a as a potential autoantigen involved in the etiology of autoimmune-mediated lacrimal gland pathogenesis . "
[Show abstract][Hide abstract] ABSTRACT: Sjögren's syndrome (SS), a systemic autoimmune disease, is characterized by inflammation of exocrine tissues accompanied by a significant loss of their secretory function. Clinical symptoms develop late and there are no diagnostic tests enabling early diagnosis of SS. Thus, particularly to study these covert stages, researchers turn to studying animal models where mice provide great freedom for genetic manipulation and testing the effect of experimental intervention. The present review summarizes current literature pertaining to both spontaneous and extrinsic-factor induced SS-like diseases in mouse models, discussing advantages and disadvantages related to the use of murine models in SS research.
[Show abstract][Hide abstract] ABSTRACT: Fas mediated apoptosis may be important in the pathogenesis of primary Sjögren's syndrome (pSS).
To examine genetic variation in the promoter region of the Fas gene in pSS.
Two single nucleotide polymorphisms at positions -1377(G/A) and -670(G/A) in the Fas gene promoter were genotyped by PCR-SSP in 101 patients with pSS and 108 Caucasoid controls.
No significant differences in allele or genotype frequencies were detected between the patients with pSS and controls. However, significant associations were observed with Ro/La autoantibody negative patients, who display milder and later onset disease. The -670A allele was more frequent in Ro/La autoantibody negative patients than in Ro/La autoantibody positive patients (p = 0.04).
This study does not confirm an earlier report of an association between pSS and the Fas promoter -670G allele. However, the results suggest that genetically determined variability in Fas expression may modulate Ro/La autoantibody responses in patients with pSS.
Annals of the Rheumatic Diseases 02/2004; 63(1):98-101. DOI:10.1136/ard.2003.006056 · 10.38 Impact Factor
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