China 
Africa 
Explore chapters and articles related to this topic
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.
Nanostructured Biointerfaces
Published in Šeila Selimovic, Nanopatterning and Nanoscale Devices for Biological Applications, 2017
Jean Paul Allain, Monica Echeverry-Rendón, Juan Jose Pavón, Sandra L. Arias
In the process of recognizing the presence of a biomaterial, the body activates different molecules such as mitogens, chemoattractants, cytokines, growth factors, and other bioactive molecules that can modulate the activity of macrophages, along with the proliferation and activation of other cell populations in the inflammatory and wound-healing responses, which are identified by the presence of mononuclear cells such as monocytes and lymphocytes, at the biomaterial implant site. Chemokines are cytokines that are chemoattractants. They coordinate cellular migration in inflammation to produce an efficient and effective process of wound healing and are involved in other processes such as hematopoiesis, angiogenesis, and cellular differentiation. The production of cytoquines such as interleukin-4 and interleukin-13 plays a significant role in the reaction of the body after exposure to a foreign agent [32,33].
Immunotherapy and Vaccines
Published in Raj Bawa, János Szebeni, Thomas J. Webster, Gerald F. Audette, Immune Aspects of Biopharmaceuticals and Nanomedicines, 2019
Johanna Poecheim, Gerrit Borchard
Unlike these observations, Henriksen-Lacey et al. described how DDA:TDB liposomes, regardless of their size, stimulated a characteristic Th1 immune response with production of IgG2 antibodies and IFN-γ (Henriksen-Lacey et al., 2011). Other reports showed that 200–600 nm particles favored induction of Th1 responses associated with higher levels of IFN-γ production, whereas microparticles of 2–8 |im in size promoted interleukin-4 (IL-4, a cytokine that induces differentiation of naive helper T cells (Th0 cells) to Th2 cells) secretion inducing humoral immunity (Kanchan and Panda, 2007).
IL-4 functionalized titanium dioxide nanotubes modulate the inflammatory response of macrophages
Published in Journal of Biomaterials Science, Polymer Edition, 2020
Xufeng Yan, Ke Shen, Qiang Tang, Xingtang Fang, Chunlei Zhang, Zhaojing Zhu, Yanhua Hou, Min Lai
Interleukin-4 (IL-4) is a cytokine secreted by type II helper T cells (Th2 cells) and plays a key role in regulating humoral immunity and adaptive immunity. It can promote the activation of macrophages into pro-healing M2-type cells and inhibit macrophages from being activated into pro-inflammatory M1-type cells. It has been reported that polypropylene mesh coated with IL-4 could successfully increase the proportion of M2 macrophages and decrease the proportion of M1 macrophages in the early stage of host reaction in mice [26]. This study intends to further modify the TNTs to promote the polarization of macrophages toward a M2 phenotype and modulate the appropriate inflammatory response to promote healing and the long-term integration of the implant with the host.