IL-17RA aptamer-mediated repression of IL-6 inhibits synovium inflammation in a murine model of osteoarthritis

Chen, L.; Li, D.Q.; Zhong, Jun; Wu, Xiaoyan; Chen, Q.; Peng, Hao; Liu, S.Q.

doi:10.1016/j.joca.2011.01.018

Cited by 57 publications

(36 citation statements)

References 33 publications

(23 reference statements)

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“…In vivo activity has been shown using a DNA L-selectin aptamer to block lymphocyte trafficking [50], multimeric OX40 or CD28 aptamers to enhance the potency of a DC-based vaccine and tumor immunity [51,52], and an IL17RA aptamer injected into inflamed joints to reduce arthritis [53,54]. The first in vivo example of using aptamers to overcome checkpoint blockade showed that a multivalent CTLA-4 aptamer (tetramer of a 35 nt aptamer linked to an adapter) could inhibit CTLA-4 and enhance tumor immunity in mice comparably to CTLA-4 antibody [55].…”

Section: Immunological Applications Of Aptamers For In Vivo Immune Cementioning

confidence: 99%

Manipulating the in vivo immune response by targeted gene knockdown

Lieberman

2015

Current Opinion in Immunology

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Aptamers, nucleic acids selected for high affinity binding to proteins, can be used to activate or antagonize immune mediators or receptors in a location and cell-type specific manner and to enhance antigen presentation. They can also be linked to other molecules (other aptamers, siRNAs or miRNAs, proteins, toxins) to produce multifunctional compounds for targeted immune modulation in vivo. Aptamer-siRNA chimeras (AsiCs) that induce efficient cell-specific knockdown in immune cells in vitro and in vivo can be used as an immunological research tool or potentially as an immunomodulating therapeutic.

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Section: Immunological Applications Of Aptamers For In Vivo Immune Cementioning

confidence: 99%

Manipulating the in vivo immune response by targeted gene knockdown

Lieberman

2015

Current Opinion in Immunology

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“…28 IL-17 mediated transduction leads to further activation and expression of pro-inflammatory cytokines such as IL-1, IL-6, and IL-8 that contribute to the inflammation. A strong correlation between the expression of IL-17 and IL-15 was observed in the SFs of RA patients but not in OA patients.…”

mentioning

confidence: 99%

Molecular targets in arthritis and recent trends in nanotherapy

Roy¹,

Kanwar²,

Kanwar³

2015

IJN

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Due to its severity and increasing epidemiology, arthritis needs no description. There are various forms of arthritis most of which are disabling, very painful, and common. In spite of breakthroughs in the field of drug discovery, there is no cure for arthritis that can eliminate the disease permanently and ease the pain. The present review focuses on some of the most successful drugs in arthritis therapy and their side effects. Potential new targets in arthritis therapy such as interleukin-1β, interleukin-17A, tumor necrosis factor alpha, osteopontin, and several others have been discussed here, which can lead to refinement of current therapeutic modalities. Mechanisms for different forms of arthritis have been discussed along with the molecules that act as potential biomarkers for arthritis. Due to the difficulty in monitoring the disease progression to detect the advanced manifestations of the diseases, drug-induced cytotoxicity, and problems with drug delivery; nanoparticle therapy has gained the attention of the researchers. The unique properties of nanoparticles make them highly attractive for the design of novel therapeutics or diagnostic agents for arthritis. The review also focuses on the recent trends in nanoformulation development used for arthritis therapy. This review is, therefore, important because it describes the relevance and need for more arthritis research, it brings forth a critical discussion of successful drugs in arthritis and analyses the key molecular targets. The review also identifies several knowledge gaps in the published research so far along with the proposal of new ideas and future directions in arthritis therapy.

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“…For the MTT assay, L929 cells treated with scFv2-CH/CL/hIL-1β proliferated at a much faster rate than those treated with Diabody-CH/CL/hIL-1β, but remarkably slower than cells treated with hIL-1β alone. Some studies have reported that IL-17A induces the release of IL-8 and IL-6 [30]. We identified that IL-6 and IL-8 of Diabody-CH/CL/hIL-17A-treated HeLa cells were lower than that of scFv2-CH/CL/hIL-17A-treated cells.…”

Section: Discussionmentioning

confidence: 66%