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Leukemias
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Rare young patients who present with hypocellular MDS benefit from immunosuppressive therapy, such as antithymocyte globulin (ATG) and cyclosporine A.130 High response rates were also observed in a study assessing the anti-CD52 antibody alemtuzumab, but the drug is no longer being developed for this indication. Clinical trials are also assessing other immune approaches through CD33 (MDSC) and Toll-like receptor signaling (TLR2).
Future and Novel Unexplored Indications of Retinoids
Published in Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish, Retinoids in Dermatology, 2019
A large case series has confirmed the beneficial effect in folliculitis decalvans (FD), where, contrary to previous reports, 82% of patients healed with isotretinoin treatment. The patients who received oral isotretinoin ≥0.4 mg/kg/day for ≥3 months responded better, and 66% of responders did not relapse during a 22-month follow-up (51). The proposed mode of action was via inhibition of neutrophil migration into the skin and a decrease in the Toll-like receptor 2 level, which mediates immune response against gram-positive bacteria. Isotretinoin also achieved modest improvement in another primary neutrophilic cicatricial alopecia—dissecting cellulitis. Of the 35 patients receiving isotretinoin (0.5–0.8 mg/kg/day), complete remission was achieved in 33 patients at 3 months, but the condition relapsed after discontinuation (52).
Effect of Nutraceuticals on Gut Microbiota—What Is the Deal in Cancer?
Published in Sheeba Varghese Gupta, Yashwant V. Pathak, Advances in Nutraceutical Applications in Cancer, 2019
Andréa Burgess, Asra Sami, Sheeba Varghese Gupta
Another advance to preserving the integrity of the gut flora rests on its protective capabilities against the cellular damage caused by cancer therapy. The mucosal barrier and innate immune system (cellular/chemical) regulates inflammation and promotes healing. The gut flora interacts with the innate immune system through Toll-like receptors, a group of proteins that broadly detect the presence of antigens. A study showed that antibiotic-treated mice were more vulnerable to small bowel injury when administered anticancer methotrexate medication. The damage to the small bowel was abrogated with the supplement of Toll-like receptor 2 ligand (Pouncey et al., 2018).
SESLA suppresses the activation of macrophages and dendritic cells after Gram-positive bacterial challenge
Published in Immunopharmacology and Immunotoxicology, 2023
Xinru Jiang, Yanwu Xu, Tiannan Xiang, Hanxiao Zhang, Xiaodong Cheng, Xiao-Dong Yang, Hongyi Hu, Xin Jiang, Yuejuan Zheng
Additionally, the KEGG pathway analysis of DEGs showed that 53 pathways were significantly enriched (p < 0.05) (Supplementary Table 3). The top 20 KEGG pathways were shown in Figure 6(B). As one of the PRRs expressed on the cell membrane, Toll-like receptor 2 (TLR2) can form a heterodimer with a similarly shaped partner TLR6. During S. aureus infection, TLR2/6 heterodimer and other intracellular PRRs (e.g. NOD2 or cryopyrin) activate immune cells upon stimulation by the components of bacteria, e.g. PGN or bacterial lipoproteins, which are considered as the main PAMPs to trigger overwhelming inflammation harmful to the host. The extracellular signal regulated kinase 1/2 (ERK1/2), c-Jun-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK) pathways and nuclear factor κB (NF-κB) pathways are common intracellular signaling pathways that are activated and lead to subsequent production of IL-6, TNF-α, IL-1β, IL-12, chemokines and IL-10, etc. [27–29]. PGN is a well-known PAMP of G+ bacteria that is mainly recognized by TLR2, NOD2 or cryopyrin in various immune cells, such as monocytes, macrophages and DCs. Therefore, to investigate the molecular regulatory mechanism by which SESLA suppresses the inflammatory response in macrophages during G+ bacterial infections, we examined the role of SESLA in the modulation of MAPK activation after PGN stimulation. As shown in Figure 6(C), the phosphorylated status of ERK, JNK and p38 was measured in primary peritoneal macrophages, and the results showed that SESLA did not affect the activation of these signaling pathways.
An overview of adapalene and benzoyl peroxide once-daily topical gel as a therapeutic option for acne
Published in Expert Opinion on Pharmacotherapy, 2021
Veronica K. Emmerich, Caitlin G. Purvis, Steven R. Feldman
Adapalene acts upon three of the four main pathogenic factors in acne: Adapalene inhibits sebum production and leads to sebaceous gland atrophy [11,26].Adapalene normalizes keratinocyte differentiation, which loosens comedones and prevents obstruction of the follicular canal [11].Adapalene decreases the expression of toll-like receptor 2 (TLR2) and activator protein-1 (AP-1) [4]. Toll-like receptors are part of the innate immune system, and TLR2 recognizes C. acnes and is responsible for propagating an inflammatory response to the bacteria [4]. AP-1 induces the synthesis of matrix metalloproteinases, which break down collagen and contribute to scarring [11].
The advantages of nanomedicine in the treatment of visceral leishmaniasis: between sound arguments and wishful thinking
Published in Expert Opinion on Drug Delivery, 2021
Kevin Matha, Brice Calvignac, Jean-Pierre Gangneux, Jean-Pierre Benoit
Another side effect observed during an AmB treatment course is the severe infusion-related toxicities. The infusion-related toxicity comprises several symptoms among them fever, rigor, nausea, vomiting, hypotension, and arthralgia [66]. This infusion toxicity is experienced by more than 2/3rd of the patients on a 2–6 hours course of AmB injection [64]. The mechanism seems to rely on the activation of the Toll-like Receptor 2 microbial pattern recognition by AmB via CD14-associated lipid rafts in mononuclear cells [67]. The activation results in the release of proinflammatory cytokines such as TNF, IL-1RA, IL-6, which serum levels elevation is correlated with the onset of the injection-related toxicity symptoms [68,69]. LAmB reduces markedly the infusion-related toxicity with lowered rates of proinflammatory cytokines (TNF, IL-1RA, IL-6) [68,69].