Predominance of IgG1 Subclass of Anti-Ro/SSA, but not Anti-La/SSB Antibodies in Primary Sjögren's Syndrome

Maran, R.; Dueymes, Maryvonne; Pennec, Y.L.; R, Casburn-Budd; Shoenfeld, Yehuda; Youinou, Pierre

doi:10.1006/jaut.1993.1032

Cited by 18 publications

(8 citation statements)

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“…With the appearance of T and B lymphocytes within the salivary and lacrimal glands, there is a subsequent production of an increasing number of detectable serum autoantibodies [31–34]. The presence of ANA, in particular anti‐SS‐A/Ro and anti‐SS‐B/La in the sera of human patients, is one parameter in the diagnosis of clinical SjS.…”

Section: Resultsmentioning

confidence: 99%

Sjögren's Syndrome‐Like Disease of C57BL/6.NOD‐Aec1 Aec2 Mice: Gender Differences in Keratoconjunctivitis Sicca Defined by a Cross‐Over in the Chromosome 3 Aec1 Locus

Nguyen

Singson²,

Kim³

et al. 2006

Scand J Immunol

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Sjögren's syndrome (SjS) is a systemic autoimmune disease in which an immunological attack primarily against the salivary and lacrimal glands results in loss of acinar cell tissue and function leading to stomatitis sicca and keratoconjunctivitis sicca. In recent years, the NOD mouse has become an accepted model of SjS, exhibiting a spontaneously developing disease that strongly mimics the human condition. Two genetic regions, one on chromosome 1 (designated Aec2) and the second on chromosome 3 (designated Aec1) of NOD mice, have been shown to be necessary and sufficient to recapitulate SjS‐like disease in non‐susceptible C57BL/6 mice. Here we describe a newly derived strain, C57BL/6.NOD‐Aec1R1Aec2, in which a recombination in Aec1 has resulted in reducing this genetic region to less than 20 cM from 48.5 cM. Profiling of this recombinant inbred strain has revealed that male mice maintain a full SjS‐like disease, whereas female mice exhibit stomatitis sicca in the absence of detectable keratoconjunctivitis sicca. These data suggest SjS‐like disease in the NOD mouse shows gender‐specific regulation determined by autosomal genes.

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Section: Resultsmentioning

confidence: 99%

Sjögren's Syndrome‐Like Disease of C57BL/6.NOD‐Aec1 Aec2 Mice: Gender Differences in Keratoconjunctivitis Sicca Defined by a Cross‐Over in the Chromosome 3 Aec1 Locus

Nguyen

Singson²,

Kim³

et al. 2006

Scand J Immunol

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“…Zouali et al reported that in SLE and mixed connective tissue disease, anti-double-stranded DNA (dsDNA) antibody was IgG1/3-dominant, and anti-RNP was IgG2-dominant [ 11 ]. Anti-Sm, anti-RNP, and anti-dsDNA in SLE [ 12 ], anti-SS-A/Ro and anti-SS-B/La in SS [ 13 ], and anti-Scl-70 in SSc [ 14 ] are reportedly IgG1-dominant. However, IgG4-type ANA was hardly detected in all the above reports.…”

Section: Discussionmentioning

confidence: 99%

Screening for IgG4-type anti-nuclear antibodies in IgG4-related disease

Kiyama

Yoshifuji

Kandou

et al. 2015

BMC Musculoskelet Disord

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BackgroundImmunoglobulin (Ig) G4-related disease (IgG4-RD) is characterized by elevated serum IgG4 and infiltration of IgG4+ plasma cells into multiple organs. It is not known whether serum IgG4 is autoreactive in IgG4-RD.MethodsWe measured anti-nuclear antibody (ANA) in 19 IgG4-RD cases, determined IgG subclasses of the ANA, and compared them with those of other systemic autoimmune diseases (systemic lupus erythematosus, Sjögren’s syndrome, systemic sclerosis, and polymyositis), using subclass-based ANA test (indirect immunofluorescence).Results58 % of IgG4-RD cases were ANA-positive (cut-off: 1:40). Whereas their subclass of ANA was predominantly IgG2, we observed no IgG4-type ANA. In systemic autoimmune diseases, subclasses of ANA were mostly IgG1, 2, or 3, but IgG4-type ANA was very rarely detected. We also found several patients in whose serum ANA patterns differed among IgG subclasses, probably due to the difference of corresponding autoantigens.ConclusionsAlthough IgG4 is highly elevated in sera of IgG4-RD patients, their ANA do not include IgG4 subclass. These results offer new insight into the role of IgG4 and the pathogenesis of IgG4-RD, implying that each IgG subclass tends to cover its own spectrum of antigens, and IgG4 is not preferentially used to make ANA.

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“…With the appearance of T and B lymphocytes within the submandibular glands of C57BL/6.NOD-Aec1Aec2 mice, plus the detectable changes within their splenic B cell populations, an increasing number of serum autoantibodies can be detected (33)(34)(35)(36). Of particular importance in human SjS disease (but not in SjS-like disease of NOD mice) are the ANAs, especially anti-SS-A/Ro and anti-SS-B/La, as the presence of these ANAs in the sera of human SjS patients is one of the diagnostic markers for clinical disease (4).…”

Section: Aec1aec2c3mentioning

confidence: 99%

Development of Sjögren’s Syndrome in Nonobese Diabetic-Derived Autoimmune-Prone C57BL/6.NOD-Aec1Aec2 Mice Is Dependent on Complement Component-3

Nguyen

Kim

Cornelius

et al. 2007

The Journal of Immunology

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The role of complement in the etiology of Sjögren’s syndrome (SjS), a human autoimmune disease manifested primarily by salivary and lacrimal gland dysfunction resulting in dry mouth/dry eye syndrome, remains ill-defined. In the present study, we examined the role of complement component-3 (C3) using a newly constructed C3-gene knockout mouse, C57BL/6.NOD-Aec1Aec2.C3−/−. Inactivation of C3 in the parental C57BL/6.NOD-Aec1Aec2 strain, a model of primary SjS, resulted in a diminished or total absence of both preclinical and clinical manifestations during development and onset of disease, including reduced acinar cell apoptosis, reduced levels of caspase-3, lack of leukocyte infiltration of submandibular glands, reduced synthesis of disease-associated autoantibodies, maintenance of normal glandular architecture, and retention of normal saliva secretion. In addition, C57BL/6-NOD.Aec1Aec2.C3−/− mice did not exhibit increased numbers of marginal zone B cells, a feature of SjS-prone C57BL/6-NOD.Aec1Aec2 mice. Interestingly, C57BL/6-NOD.Aec1Aec2.C3−/− mice retained some early pathological manifestations, including activation of serine kinases with proteolytic activity for parotid secretory protein. This improvement in the clinical manifestations of SjS-like disease in C57BL/6.NOD-Aec1Aec2.C3−/− mice, apparently a direct consequence of C3 deficiency, supports a much more important role for complement in the adaptive autoimmune response than previously recognized, possibly implicating an essential role for innate immunity.

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Predominance of IgG1 Subclass of Anti-Ro/SSA, but not Anti-La/SSB Antibodies in Primary Sjögren's Syndrome

Cited by 18 publications

References 0 publications

Sjögren's Syndrome‐Like Disease of C57BL/6.NOD‐Aec1 Aec2 Mice: Gender Differences in Keratoconjunctivitis Sicca Defined by a Cross‐Over in the Chromosome 3 Aec1 Locus

Sjögren's Syndrome‐Like Disease of C57BL/6.NOD‐Aec1 Aec2 Mice: Gender Differences in Keratoconjunctivitis Sicca Defined by a Cross‐Over in the Chromosome 3 Aec1 Locus

Screening for IgG4-type anti-nuclear antibodies in IgG4-related disease

Development of Sjögren’s Syndrome in Nonobese Diabetic-Derived Autoimmune-Prone C57BL/6.NOD-Aec1Aec2 Mice Is Dependent on Complement Component-3

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