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Портал Begell Электронная Бибилиотека e-Книги Журналы Справочники и Сборники статей Коллекции
Journal of Long-Term Effects of Medical Implants
SJR: 0.133 SNIP: 0.491 CiteScore™: 0.89

ISSN Печать: 1050-6934
ISSN Онлайн: 1940-4379

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Journal of Long-Term Effects of Medical Implants

DOI: 10.1615/JLongTermEffMedImplants.2014011295
pages 243-251

Role of Innate Immune Sensors, TLRs, and NALP3 in Rheumatoid Arthritis and Osteoarthritis

Yuya Takakubo
Department of Orthopaedic Surgery, Yamagata University Faculty of Medicine, Iida-Nishi 2-2-2, Yamagata, 990-9585, Japan
G. Barreto
Department of Clinical Medicine, University of Helsinki and ORTON Orthopaedic Hospital of the Invalid Foundation, Helsinki, Finland
Yrjo T. Konttinen
Department of Orthopaedics, Teaching Hospital, Faculty of Medicine and Dentistry, Palacky University, Olomouc, Czech Republic; Department of Orthopaedics, ORTON Orthopaedic Hospital, 00280 Helsinki, Finland; COXA Hospital for Joint Replacement, 33520 Tampere, Finland
H. Oki
Department of Orthopaedic Surgery, Yamagata University Faculty of Medicine, Yamagata, Japan
Michiaki Takagi
Department of Orthopaedic Surgery, Yamagata University Faculty of Medicine, Iida-Nishi 2-2-2, Yamagata, 990-9585, Japan

Краткое описание

Innate immune sensors, Toll-like receptors (TLRs), and nucleotide-binding oligomerization domain-like receptors (NLRs) participate in the induction of innate inflammatory and adaptive immune responses in rheumatoid arthritis (RA) and osteoarthritis (OA). Danger signals, e.g., heat-shock proteins (HSPs) and high mobility group box-1 protein (HMGB-1), internal ligands of TLRs, have been reported in the patients with RA and OA. In RA, TLR1−9 have been implicated in the pathogenesis. Although the precise role of each receptor is still unknown, immunohistochemical analyses of RA tissues after treatment of biologic disease modifying antirheumatic drugs showed phenotypic changes of immune cell types and residual expression of some TLRs. This suggests the potential for modulation of moderate/severe local joint inflammation, composed in particular of and possibly driven by the "auto-inflammatory" TLR+ cells, still responding to internal ligands derived from destroyed tissues. In OA, systematic profiling of TLR using a histological grading system recently showed that TLR+ cells are greater in number in the surface zone of grades 3 and 4 OA, but interestingly not grade 5. NACHT, LRR, and PYD domains-containing protein (NALP) 3 and related molecules have been also demonstrated both in RA and OA. In addition, a cross talk mechanism of TLR and NALP responsible for increasing joint inflammation has been suggested. Taken together, although OA is not basically an inflammatory disease, and is different from that of RA, pattern recognition receptors-signaling pathways, TLRs and NALP3 may play a role in the pathogenesis of both these conditions, probably as driving forces of progression. Precise and intensive analyses of both receptors, signal pathways, and cross talk mechanisms may provide a new therapeutic approach as molecular targets.