Expression of innate immune receptors in the immunopathologic lesion of primary Sjogren's syndrome: preliminary results

Toll-like receptors (TLRs) have a crucial role in early host defence against invading pathogens. They recognize specific molecular patterns that are present in microbial and viral components, whereas several endogenous molecules seem to be placed among their expanding group of ligands. The CD91 receptor (low-density lipoprotein receptor-related protein [LRP1] or alpha 2-macroglobulin receptor [A2MR]) is a multifunctional receptor that recognizes hsp-chaperoned peptides, which are processed and presented by the MHC class I and MHC class II molecules. So far, there is an increasing evidence that the receptors of innate immunity also play an important role in acquired immunity.

The objective of our study was to evaluate the expression of TLRs and CD91 in minor salivary gland (MSG) biopsy tissues and non-neoplastic salivary gland epithelial cell lines obtained from patients with primary Sjogren's syndrome (pSS).

At the mRNA level, the expression of TLR2, TLR4, TLR7, TLR9 and CD91 was examined in a non-neoplastic salivary gland epithelial cell line from a patient with pSS by means of RT-PCR. Protein expression of TLR2, TLR4 and CD91 was studied by immunohistochemistry in MSG biopsy tissues from 12 patients with pSS and nine control patients with non-specific sialadenitis.

RT-PCR analysis revealed transcriptional activation of TLR2, TLR4, TLR7, TLR9 and CD91 genes in the epithelial cell line of pSS patient. In MSG biopsy tissues, abundant expression of CD91 was observed in ductal cells of both pSS and control tissues, but also in the focal lymphocytic infiltrates of pSS patients. TLR2 and TLR4 protein expression was localized in single, scattered cells, both in pSS patients and, to a lesser extent, in control patients, showing a distinct staining pattern.

The presence of CD91 and TLRs in the immunopathologic lesion of Sjogren's syndrome provides preliminary evidence, suggesting their possible role in innate immune responses within the lesion.