Regular ArticleTh1 Predominance and Perforin Expression in Minor Salivary Glands from Patients with Primary Sjögren's Syndrome
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Programmed Cell Death-1 Pathway Deficiency Enhances Autoimmunity Leading to Dacryoadenitis of Mice
2021, American Journal of PathologyUnique glandular ex-vivo Th1 and Th17 receptor motifs in Sjögren's syndrome patients using single-cell analysis
2018, Clinical ImmunologyCitation Excerpt :There are two shared public clonal TCR motifs between controls and pSS patients (CFLFLSMSACVW and SVGSTAIPP*T); there are two unique TCR motifs in pSS (CVVSDTVLETAGE and LSTD*E). Earlier studies using gene expression and immunostaining demonstrated that Th1 and IFN-γ were elevated in the LSG, which positively correlated with high infiltration scores and longer disease duration in patients [33–35]. Additionally, SS patients who developed lymphoma exhibited even higher Ifn-γ transcripts compared to both (non-lymphoma) SS and healthy controls [36].
Analysis of IL10 haplotypes in primary Sjögren's syndrome patients from Western Mexico: Relationship with mRNA expression, IL-10 soluble levels, and autoantibodies
2015, Human ImmunologyCitation Excerpt :High IL10 expression levels were found in pSS patients in our study. Previous works showed high IL10 mRNA expression in salivary glands of pSS patients [49–52]. Furthermore, Fox et al. suggested that salivary gland CD4+ T cells produce over 40-fold more IL10 mRNA than peripheral blood CD4+ T cells from the same patient or normal controls, moreover, increased levels of IL-10 were found in saliva of pSS patients suggesting that the elevated mRNA levels detected in their glandular tissue correlated with local protein synthesis [49].
T helper subsets in Sjögren's syndrome and IgG4-related dacryoadenitis and sialoadenitis: A critical review
2014, Journal of Autoimmunity
- f1
ECK and PR contributed equally to this work.
- f2
Correspondence to: Joaquı́n Coll, Department of Medicine, Hospital del Mar, Passeig Marı́tim 25–29, 08003 Barcelona, Spain. Fax: 34 93 221 2453. E-mail:[email protected]