Sammanfattning
Oral lichenoid reactions (OLRs) are chronic inflammatory lesions induced by contact with allergens. Toll-like receptors (TLRs) are members of pattern-recognition receptors superfamily. Once activated, TLRs induce production of cytokines and chemokines thus leading to inflammatory reaction in host tissue. In the present study, we aimed to investigate the potential role of TLRs in the initiation and perpetuation of OLRs, in which TLRs induce innate immune responses mounted against allergens. TLRs, one through 10, were mapped in tissue samples obtained from healthy donors and OLR patients using real-time quantitative reverse transcription PCR, immunostaining and image analyses. We found that the immunoreactivity for all TLRs was increased in OLRs, except for TLR5 which was noticeably reduced. Gene analysis revealed that TLR1, TLR2, TLR4, TLR7, TLR8 and TLR9 transcripts were upregulated in OLRs compared with controls. In contrast, expression of TLR3, TLR5 and TLR6 genes were
negatively regulated in OLRs. TLR10 remained unchanged in both groups. In
conclusion, TLRs expression is deranged in OLRs in which TLRs could be sensitized by allergens and haptens derived from dental restorations. TLR-reactivity is further enhanced by recruitment of T-lymphocytes forming a diffuse lymphocytic infiltrate and thus creating a pro-inflammatory loop-cycle.
These findings suggest that TLRs are involved in OLRs and pave the way for alternative cost-effective therapeutic interventions.
negatively regulated in OLRs. TLR10 remained unchanged in both groups. In
conclusion, TLRs expression is deranged in OLRs in which TLRs could be sensitized by allergens and haptens derived from dental restorations. TLR-reactivity is further enhanced by recruitment of T-lymphocytes forming a diffuse lymphocytic infiltrate and thus creating a pro-inflammatory loop-cycle.
These findings suggest that TLRs are involved in OLRs and pave the way for alternative cost-effective therapeutic interventions.
Originalspråk | engelska |
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Tidskrift | American Journal of Dermatopathology |
Volym | 39 |
Utgåva | 11 |
Sidor (från-till) | 811-818 |
Antal sidor | 8 |
ISSN | 0193-1091 |
DOI | |
Status | Publicerad - 2017 |
MoE-publikationstyp | A1 Tidskriftsartikel-refererad |
Vetenskapsgrenar
- 313 Odontologi