Journal
FRONTIERS IN IMMUNOLOGY
Volume 7, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2016.00022
Keywords
innate immunity; Toll-like receptor 7; Interferon-alpha; systemic lupus erythematosus; pathogenesis
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Funding
- CONACYT (National Council of Science and Technology) [RONSEC SALUD 2010-1-139788]
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Background: Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease involving multiple organs. It is currently accepted that several genetic, environmental, and hormonal factors are contributing to its development. Innate immunity may have a great influence in autoimmunity through Toll-like receptors. TLR-7 recognizing single-strand RNA has been involved in SLE. Its activation induces intracellular signal with attraction of MyD88 and NF-kBp65, leading to IFN-alpha synthesis which correlate with disease activity. Objective: To assess the expression of TLR-7, MyD88, and NF-kBp65 in B lymphocytes of Mayan women with SLE. Methods: One hundred patients with SLE and 100 healthy controls, all of them Mayan women, were included. TLR-7 was analyzed on B and T lymphocytes, and MyD88 and NF-kB only in B lymphocytes. Serum INF-alpha level was evaluated by ELISA. Results: Significant expression (p < 0.0001) of TLR-7 in B and T lymphocytes and serum IFN-alpha increased (p = 0.034) was observed in patients. MyD88 and NF-kBp65 were also increased in B lymphocytes of patients. TLR-7 and NF-kBp65 expression correlated, but no correlation with INF-alpha and disease activity was detected. Conclusion: Data support the role of TLR-7 and signal proteins in the pathogenesis of SLE in the Mayan population of Yucatan.
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