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Interleukin 12: A Potent Vaccine Adjuvant for Promoting Cellular Immunity and Modulating Humoral Immunity
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Interleukin 12 (IL-12) is a unique cytokine produced by antigen presenting cells. As discussed in more detail in several recent reviews [1–3], among the activities of IL-12 are several which bear on its potential as a vaccine adjuvant for both promoting cellular immune responses and modulating and enhancing humoral responses. One of the most potent activities of IL-12 is induction of 7-interferon (IFN-7) from T and natural killer (NK) cells. Enhancement of antigen presentation and suppression of T helper 2 (Th2) cell development by IFN-7 play key roles in promoting and directing the immune response developed in the presence of IL-12. Interleukin-12 also specifically and uniquely promotes the differentiation of T helper progenitors to be come Th1 cells. In both mice and humans at least two classes of T helper cell subsets that exert specific effects on immune development develop. T helper 1 (Th1) cells express IFN-7 and IL-2 cytokines that promote a cellular immune response by activating macrophage and enhancing development and expansion of CD8+ effector cells. Th2 cells express IL-4 and IL-5 and lack expression of IFN-7 and IL-2. As a consequence, Th2 cells promote the differentiation of B cells to express noncytophilic antibodies (e.g., immunoglobulin G1 [IgG 1] in mice) and IgA and recruit eosinophils. Although IL-12 has only moderate activity in promoting proliferation of primed T cells, costimulation with accessory molecules such as B7.1 has been shown dramatically to enhance proliferation of CD4+ and CD8+ T cells induced by IL-12 [4].
Anti-infectious innate and adaptive immune responses
Published in Gabriel Virella, Medical Immunology, 2019
Carl Atkinson, Gabriel Virella
Interleukin-12. In conjunction with nitric oxide, IL-12 stimulates the cytotoxic activity of NK cells, enhancing their release of interferon-γ. Interferon-γ and IL-12 also have an important role in promoting Th1 lymphocyte differentiation.
Non-melanoma skin cancer
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2014
Stephen L. Morris, Sean Whittaker, Margaret Spittle
Small cohort studies have reported that interleukin-12 (IL-12) and interferon-a can produce clinical responses but their role remains to be established. Cyclosporine is contraindicated as it may cause disease progression.227–228
TBC and COVID: an interplay between two infections
Published in Expert Opinion on Drug Safety, 2023
Giuseppe Murdaca, Francesca Paladin, Gloria Mangini, Debora Tiso, Sebastiano Gangemi
A key role in the immune response against mycobacterium is played by alveolar macrophages [19]. Phagocytosis of M. tuberculosis is mediated by binding to complement receptors, mannose receptor (MR), surfactant molecules, and DC-SIGN (dendritic cell-specific intracellular adhesion molecule-3–grabbing nonintegrin). In the recognition of M. tuberculosis are also involved Toll-like receptors (TLRs), C-type lectin receptors (CLRs), and Nod-like receptors (NLRs), expressed by alveolar macrophages [20]. M. tuberculosis inhibits macrophage activation and becomes highly resistant to elimination through several strategies, including inhibition of phago-lysosome fusion, detoxification of nitrogen and oxygen radicals [21]. In response to M. tuberculosis infection, macrophages secrete interleukin 12 (IL-12) and TNF-α [22]. These cytokines increase local inflammation with the recruitment of T cells and natural killer (NK) cells to the area of infected macrophages, inducing the differentiation of T cells into TH1 cells (T-helper cells), resulting in the secretion of interferon gamma (IFN-γ) [23]. In the presence of IFN-γ, infected macrophages are activated, leading to increased phagosome-lysosome fusion and intracellular killing [24]. In addition, TNF-α stimulates the production of nitric oxide and related reactive nitrogen intermediates, leading to enhanced intracellular killing [25].
Oral administration of Bifidobacterium breve promotes antitumor efficacy via dendritic cells-derived interleukin 12
Published in OncoImmunology, 2021
Qingxiang Li, Yuke Li, Yifei Wang, Le Xu, Yuxing Guo, Yixiang Wang, Lin Wang, Chuanbin Guo
Since the association between gut microbiota and cancer immunotherapy gradually uncovered, some important cytokines and immune cells have been noticed. Interleukin 12 (IL-12), produced by inflammatory myeloid cells, is a kind of heterodimeric cytokines with proinflammatory properties.16 IL-12 polarizes naive helper T cells (Th) to Th1 type and stimulates CD8+ T cells and NKT cells.17 Clinical studies based on IL-12 achieved well response, which mainly focused on local gene therapy.18 Current studies indicated that IL-12 promoted the curative effect of CTLA-4 or PD-1 blockade17,19,20 and adoptive cell therapy.21 Dendritic cells (DCs) are important source of endogenous IL-12. It was reported that effective anti-PD-1 immunotherapy requires intratumoral DCs-derived IL-12.19 And conventional type 1 DCs-derived IL-12 was necessary to the priming of follicular helper T cells, which was vitally important for the efficacy of chemotherapy for proximal colon cancer.22 All these evidence suggest the crucial role of IL-12 in immunotherapy against solid tumor.
Mogamulizumab in the treatment of advanced mycosis fungoides and Sézary syndrome: safety and efficacy
Published in Expert Review of Anticancer Therapy, 2020
Daniel J. Lewis, Alain H. Rook
There is significant rationale for pairing mogamulizumab with various agents that stimulate the immune response. For example, interferon-alpha (IFN-α) and -gamma (IFN-γ) promote the ADCC induced by mogamulizumab against CCR4+ Sézary cells. Specifically, they stimulate NK cell maturation, memory, priming, and tumor surveillance in addition to activating NK cells to a high level of cytotoxicity [37]. In one report by Patino et al, combining mogamulizumab and pegylated IFN-α2a resulted in PRs in 3 of 3 patients after only two weeks of therapy and CRs after two months [38]. Besides interferons, there is a strong immunologic basis for concomitant interleukin-12 (IL-12) and mogamulizumab, as IL-12 stimulates NK cells to produce IFN-γ and augments NK cell proliferation and cytolytic activity [39–41]. Lastly, topical Toll-like receptor (TLR) agonists such as imiquimod or resiquimod activate NK cells and induce dendritic cells to produce both IFN-α and IL-12, thus exerting a more potent anti-tumor response via ADCC [42,43]. Although combining immunotherapeutic agents may enhance efficacy, this approach may also increase the risk of immune-related adverse events, as has been observed when combining mogamulizumab with a PD-1 inhibitor [44].