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Anti-Arthritic Potential of Gold Nanoparticle
Published in Klaus D. Sattler, st Century Nanoscience – A Handbook, 2020
Jayeeta Sengupta, Sourav Ghosh, Antony Gomes
When T lymphocyte interacts with MHC on antigen-presenting cells, it may be activated, or show tolerance to the antigen, or undergo programmed cell death, depending on a second signal through appointing additional cellular receptors. The CD24 molecule on the T-cell surface may act as this second signal of costimulation. Activated T cells proliferate and secrete additional cytokines such as interleukin-2, interleukin-4, tumor necrosis factor, and interferon-γ. Interleukin-2 amplifies the proliferation of T cells. Very early inflamed synovium has been found to have an unexpected T helper cell profile, along with increased expression of interleukin-4, interleukin-5, and interleukin-13. When the diseased is established, synovial T cells produce low amounts of interferon-γ, interleukin-10, and tumor necrosis factor-α, while interleukin-2 and interleukin-4 become virtually absent. Interleukin-17 is produced spontaneously in synovial cells of rheumatoid arthritis patients. Interleukin-23 promotes the survival and proliferation of T helper cells. The receptor for interleukin-17 is expressed all over the synovium and exerts pleiotropic effects. Thus, T-cell-derived interleukin-17 (subtypes 17A and 17F) promotes monocyte-dependent interleukin-1 and tumor necrosis factor-α production and induces osteoclast differentiating factor RANKL (receptor activator of nuclear factor kappa-B ligand), stimulating synovial fibroblasts to express interleukin-6, interleukin-8, granulocyte colony-stimulating factor, prostaglandin E2, and matrix metalloproteinases.
Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
They who showed the B. burgdorferi–vaccinated interferon gamma–deficient (IFN-γo mice challenged with the Lyme spirochete) developed a prominent chronic severe destructive osteorthropathy. The immune response underlying the development of the severe destructive arthritis involves interleukin-17 (IL-17). Treatment of vaccinated IFN-γo mice challenged with B. burgdorferi with anti-IL-17 antibody delayed the onset of swelling of the hind paws, but more importantly, inhibited the development of arthritis. Histopathologic examination confirmed that treatment with anti-IL-17 antibody prevented the destructive arthopathy seen in vaccinated and challenged IFN-γo mice. Similar preventive results were obtained when vaccinated and challenged IFN-γo mice were treated with anti-IL-17 receptor antibody or sequentially with anti-IL-17 antibody followed by anti-IL-17 receptor antibody. In contrast, treatment of vaccinated IFN-γo mice with recombinant IL-17 (rIL-17) did not alter the development and progression of arthritis found in vaccinated and challenged IFN-γo mice without treatment with rIL-17. Therapeutic intervention may be a realistic approach to prevent arthritis especially if IL-17 is involved in the perpetuation of chronic or intermittent arthritis.
Understanding the complex microenvironment in oral cancer: the contribution of the Faculty of Dentistry, University of Otago over the last 100 years
Published in Journal of the Royal Society of New Zealand, 2020
Alison Mary Rich, Haizal Mohd Hussaini, Benedict Seo, Rosnah Bt Zain
Interleukin 17 is a pro-inflammatory cytokine with both pro- and anti-tumour effects which has been shown to have increased expression in some cancers. Its pro-tumour effects are mediated by mechanisms including inducing the expression of matrix metalloproteinases (MMPs) in tumour cells and/or stimulating increased tumour angiogenesis. The anti-tumour effects of IL17 are exerted through increased Tc cells and IFNγ activity. Our studies showed significantly more IL17+ cells were present in the TME of OSCC than inflammatory controls (Avadhani 2015). Double-labelling immunofluorescence studies revealed that Th cells, Tc cells, macrophages and mast cells co-expressed IL17 (Avadhani et al. 2017). Using an extracellular matrix (ECM) cell invasion assay kit with invasion assay chambers we found that IL17 significantly promoted the in vitro invasion of OSCC cell lines (Avadhani 2015). These results are consistent with the observations in other cancers where IL17 was found to facilitate tumour progression e.g. breast cancer cell lines, cervical cancer cell lines (Cochaud et al. 2013; Punt et al. 2015).