siRNA-mediated targeting of hepatocyte mannan-binding lectin-associated serine protease-3 for the treatment of murine collagen-antibody-inducsed arthritis (CAIA), a model for human rheumatoid arthritis

Banda, Nirmal K.; Desai, Dhruv; Casterano, Adam; Scheinman, Robert I.; Acharya, Sumitra; Sekine, Hideharu; Fujita, Teizo; Hansen, Annette G.; Thiel, Steffen; Borodovsky, Anna; Holers, V. Michael

doi:10.1016/j.molimm.2017.06.129

Cited by 1 publication

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“…Given that MASP-1 and MASP-3 are splice variants derived from a single MASP-1/3 gene, it has been difficult to separate the two functionally. Nonetheless, our most recent data suggest that MASP-3, compared with MASP-1 or MASP-2, is the main driver of the AP and thus CAIA ( 271 ). In these studies, MASP-3 siRNA inhibited CAIA compared with MASP-1 or MASP-2 siRNAs ( 271 ).…”

Section: Mouse Models Of Human Rheumatoid Arthritismentioning

confidence: 87%

“…Nonetheless, our most recent data suggest that MASP-3, compared with MASP-1 or MASP-2, is the main driver of the AP and thus CAIA ( 271 ). In these studies, MASP-3 siRNA inhibited CAIA compared with MASP-1 or MASP-2 siRNAs ( 271 ). All of the above, in vivo CAIA studies, show that MASP-3 proteases of the LP regulate the AP, a finding that has also been confirmed by using in vitro studies by various research groups ( 44 , 45 , 265 , 268 , 272 ).…”

Section: Mouse Models Of Human Rheumatoid Arthritismentioning

confidence: 87%

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Complement in the Initiation and Evolution of Rheumatoid Arthritis

2018

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The complement system is a major component of the immune system and plays a central role in many protective immune processes, including circulating immune complex processing and clearance, recognition of foreign antigens, modulation of humoral and cellular immunity, removal of apoptotic and dead cells, and engagement of injury resolving and tissue regeneration processes. In stark contrast to these beneficial roles, however, inadequately controlled complement activation underlies the pathogenesis of human inflammatory and autoimmune diseases, including rheumatoid arthritis (RA) where the cartilage, bone, and synovium are targeted. Recent studies of this disease have demonstrated that the autoimmune response evolves over time in an asymptomatic preclinical phase that is associated with mucosal inflammation. Notably, experimental models of this disease have demonstrated that each of the three major complement activation pathways plays an important role in recognition of injured joint tissue, although the lectin and amplification pathways exhibit particularly impactful roles in the initiation and amplification of damage. Herein, we review the complement system and focus on its multi-factorial role in human patients with RA and experimental murine models. This understanding will be important to the successful integration of the emerging complement therapeutics pipeline into clinical care for patients with RA.

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Section: Mouse Models Of Human Rheumatoid Arthritismentioning

confidence: 87%