Sjögren's research encompasses vital topics such as the causes, subtypes, biomarkers, genetics, antibodies, and progression.
Expression of interleukin-17 in primary Sjögren's syndrome (pSS) and the correlation with disease severity: A systematic review and meta–analysis. The expression of IL-17 is obviously increased in patients with pSS, especially among those without immunosuppressive treatment. PubMed, Scand J Immunol, 2018 Apr;87(4):e12649. (Also see Interleukins)
Deterioration in saliva quality in patients with Sjögren's syndrome (SS): impact of decrease in salivary epidermal growth factor on the severity of intraoral manifestations. The deterioration in saliva quality as well as lower intraoral clearance by hyposalivation could play a role in the pathogenesis of refractory intraoral manifestations in patients with SS. PubMed, Inflamm Regen, 2018 Apr 9;38:6.
B-cell activity markers are associated with different disease activity domains in primary Sjögren's syndrome. All biomarkers were associated with total EULAR Sjögren's Syndrome Disease Activity Index scores but with differing domain associations. PubMed, Rheumatology (Oxford), 03/28/2018. (Also see B cells and T cells)
Genetics in Sjögren's Syndrome. The genes associated with Sjögren syndrome (SS) can be assigned to the NF–kB pathway, the IFN signaling pathway, lymphocyte signaling, and antigen presentation. Rheumatic Disease Clinics, 06/21/2016.
Impact of the leucocyte immunoglobulin-like receptor A3 (LILRA3) on susceptibility and subphenotypes of systemic lupus erythematosus (SLE) and Sjögren's syndrome (pSS). Functional LILRA3 is a new susceptibility factor for SLE and pSS and it highly predisposes to certain phenotypes such as leucopenia, thrombocytopenia and autoantibody-positive subphenotypes. PubMed, Ann Rheum Dis, 2015 Nov;74(11):2070-5. (Also see Research on Systemic Lupus Erythematosus)
Update on the immunobiology of Sjögren's (pSS) syndrome. Progress made during the last few years on the pathogenesis of pSS has been mirrored by clinical trials directed at inhibiting cytokines, B, or T cell responses. PubMed, Current Opinion in Rheumatology, 08/04/2015. (Also see B cells and T cells)
Novel and rare functional genomic variants in multiple autoimmune syndrome (MAS) and Sjögren's syndrome. The LRP1/STAT6 novel mutation has the strongest case for being categorised as potentially causative of MAS given the presence of intriguing patterns of functional interaction with other major genes shaping autoimmunity. PubMed, J Transl Med, 2015 Jun 2;13:173. (Also see Multiple Autoimmune Syndrome)
A review of salivary gland histopathology in primary Sjögren's syndrome with a focus on its potential as a clinical trials biomarker. The role of histopathology as a biomarker for stratification and response to therapy is reviewed. PubMed, Ann Rheum Dis, 06/01/2015.
Salivary mucins induce a Toll-like receptor 4 (TLR4)-mediated pro-inflammatory response in human submandibular salivary cells: are mucins involved in Sjögren's syndrome (SS)? Salivary mucins were recognized by TLR4 in epithelial cells initiating a pro-inflammatory response and thereby contribute to the development of a chronic state characteristic of SS. PubMed, Rheumatology (Oxford), 03/22/2015.
Etiopathogenic Role of Surfactant Protein D (SP-D) in the Clinical and Immunological Expression of Primary Sjögren Syndrome (pSS). High SP-D levels were found with severe glandular involvement, hypergammaglobulinemia, leukopenia, extraglandular manifestations, and positive anti-Ro/La antibodies. PubMed, J Rheumatol, J Rheumatol, 2015 Jan;42(1):111-8.
Sjögren's Antibodies (Anti-SS-A/Anti-SS-B). SS-A(Ro) is found in 60% to 70% of patients with Sjögren's syndrome and 30% to 40% of patients with SLE. SS-B(La) is found in 50% to 60% of Sjögren's syndrome and 10% to 15% of SLE. LabCorp.
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