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Transplantation
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Jonathon Olsburgh, Rhana H. Zakri
BasiliximabHumanised or chimeric monoclonal anti-CD25 antibody.Interleukin-2 receptor inhibitor/antagonist.Prevents T-cell activation and proliferation.Administered intravenously.Given at induction and on day 4 post-transplant.
Host-Directed and Immune-Based Therapies for Human Immunodeficiency Virus Infection
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Hernan Valdez, Michael M. Lederman, Bharat Ramratnam, Timothy P. Flanigan
In summary, many cytokines could prove helpful in reconstituting immune function or decreasing viral replication. Interleukin 2, the one most extensively tested, should be evaluated in a phase III clinical trial, the design of which is problematic, as discussed earlier. Cytokines in earlier stages of clinical trial development pose other questions: How useful is HIV RNA as a surrogate marker when using immune-based therapies? Will cytokine therapy or cytokine inhibition provide any additional benefit to highly active antiretroviral therapy?
Toxoplasma gondii
Published in Peter D. Walzer, Robert M. Genta, Parasitic Infections in the Compromised Host, 2020
Recombinant interleukin 2 facilitates the development of cytotoxic T cells (390) and natural killer cell activity (391) as well as antigen-induced T-cell proliferation (392). Chan and Luft (388) showed that splenocytes from animals acutely infected with T. gondii had a diminished capacity to produce interleukin 2. Sharma et al. (393) has recently demonstrated that administration of interleukin 2 (IL2) significantly protected mice against mortality due to a lethal infection with T. gondii. Administration of IL2 enhanced survival and reduced the number of cysts formed in the brain of infected animals. There was no difference in antibody synthesis specific to T. gondii or reversal in the suppression of lymphocyte transformation associated with acute infection. However, natural killer cell activity was potentiated in mice that received interleukin 2. Administration of interleukin 2 may prove useful as adjunctive therapy or as a method to specifically restore a particular defect in selected immunocompromised hosts.
Treatment of inflammatory complications in common variable immunodeficiency (CVID): current concepts and future perspectives
Published in Expert Review of Clinical Immunology, 2023
T cells in CVID are not only activated, they are also exhausted, as indicated in a study from our group where patients with GLILD had high levels of soluble CD25, IFN-gamma and TNF, but also of the T-cell exhaustion marker soluble TIM3 [127]. Exhausted T cells have low proliferative capacity, a consistent feature of CVID that has been known for decades, and with some studies presenting therapeutic measures to enhance the proliferative potential of T cells. Our group showed in the late 90ties that the low proliferation of T cells in CVID could be partially reversed by inhibitors of cyclic AMP in vitro [128]. Interleukin-2 (IL-2) is a strong inducer of T-cell growth and proliferation. Cunningham-Rundles and her colleagues tried giving CVID-patients low dose interleukin-2 and showed not only that T cells from patients improved their proliferative capacity, but that there also was an increase in immunoglobulin levels [129].
Simlukafusp alfa (FAP-IL2v) immunocytokine is a versatile combination partner for cancer immunotherapy
Published in mAbs, 2021
Inja Waldhauer, Valeria Gonzalez-Nicolini, Anne Freimoser-Grundschober, Tapan K Nayak, Linda Fahrni, Ralf J. Hosse, Danny Gerrits, Edwin J. W. Geven, Johannes Sam, Sabine Lang, Esther Bommer, Virginie Steinhart, Elisabeth Husar, Sara Colombetti, Erwin Van Puijenbroek, Markus Neubauer, J. Mark Cline, Pradeep K. Garg, Gregory Dugan, Federica Cavallo, Gonzalo Acuna, Jehad Charo, Volker Teichgräber, Stefan Evers, Otto C. Boerman, Marina Bacac, Ekkehard Moessner, Pablo Umaña, Christian Klein
Interleukin-2 (IL-2) is a cytokine produced primarily by activated T cells that plays a critical function in the generation, differentiation, survival, and homeostasis of immune effector cells.1,2 IL-2 signaling is mediated by binding to the IL-2 receptor (IL-2 R), which consists of up to three individual subunits, α (CD25), β (CD122), and γ (CD132).1 The low-affinity dimeric IL-2 Rβγ form is expressed on natural killer (NK) cells, monocytes, macrophages, and resting CD4+ and CD8+ T cells.1,2 The high-affinity trimeric IL-2 Rαβγ is transiently induced on activated NK cells and CD4+ and CD8+ T cells. IL-2 functions to expand T cell populations in an autocrine fashion, differentiate antigen-activated CD4+/CD8+ T cells into effector T cell subsets, and activate NK cells.2 Activation of innate and adaptive immune effector cells in this manner is the basis for using IL-2 to stimulate an anti-tumor response.3–5 However, to counteract autoimmunity, IL-2 also has immunosuppressive properties and is involved in peripheral immune tolerance mediated by CD4+ FOXP3+ regulatory T cells (Tregs), which constitutively express high levels of IL-2 Rα.2,6,7 Tregs suppress T cell activity, thereby compromising anti-tumor immunity.8 IL-2 is also essential for activation-induced cell death (AICD) of activated T cells by upregulating the expression of Fas ligand and downregulating apoptosis inhibitors.9,10
IL-2 regulates oral mucosa inflammation through inducing endoplasmic reticulum stress and activating the NF-ĸB pathway
Published in Journal of Receptors and Signal Transduction, 2020
More than 80% of the population worldwide will experience an episode of oral mucosa inflammation, which now remains as a costly condition today during lifetime [1,2]. Oral mucosa inflammation is a major pathological process that is regulated by many factors such as oxidative stress, infection, injuries, and other diseases [3,4]. Oral mucosa inflammation is a pathologic condition associated with oral epithelium damage that is also the major cause of pain in oral [5,6]. A variety of different molecular mechanisms have been reported including abnormal changes in genes and exposure to environmental chemicals, oxidative stress, and cell apoptosis. Research attempts in many different models have been made to obtain better understanding of the development of oral mucosa inflammation and cellular biology events involved [8,9]. Oral mucosa inflammation is commonly characterized by the loss of cell number in the oral epithelium [10,11]. Prior studies of oral mucosa inflammation suggested that interleukin seems to play an important role in regulating oral mucosa inflammation. However, the molecular mechanism underlying this remains unknown. In the present study, we explore the influence of interleukin-2 (IL-2) on oral mucosa inflammation [12].