2014
DOI: 10.1016/j.intimp.2014.02.038
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TGF-β/Smad signaling pathway regulates Th17/Treg balance during Echinococcus multilocularis infection

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Cited by 70 publications
(49 citation statements)
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“…Furthermore, IL-17R-deficient mice were associated with reduced production of the chemokine MIP-2 along with the suboptimal levels of neutrophil recruitment and higher parasitic load as compared with wild-type counterparts 111 . Additionally, during echinococcosis, IL-17 plays a crucial immune protective role by regulating the Tregs which are associated with tolerance during infection 112 . In contrast, in human cutaneous leishmaniasis 113115 and Eimeria tenella infection in chickens 116 , IL-17 contributed to the pathology through excessive inflammation and subsequent tissue damage.…”
Section: Role Of Il-17 In Parasitic Infectionmentioning
confidence: 99%
“…Furthermore, IL-17R-deficient mice were associated with reduced production of the chemokine MIP-2 along with the suboptimal levels of neutrophil recruitment and higher parasitic load as compared with wild-type counterparts 111 . Additionally, during echinococcosis, IL-17 plays a crucial immune protective role by regulating the Tregs which are associated with tolerance during infection 112 . In contrast, in human cutaneous leishmaniasis 113115 and Eimeria tenella infection in chickens 116 , IL-17 contributed to the pathology through excessive inflammation and subsequent tissue damage.…”
Section: Role Of Il-17 In Parasitic Infectionmentioning
confidence: 99%
“…Phosphorylated Smads translocate to the nucleus where they function as transcription factors, initiating target gene transcription (Banas et al, 2006). The relationship between the TGF-␤/Smad pathway, and especially the expression of Smad7, which may play a regulatory role in the system, and clinical and/or pathological features of AE in experimental models as well as in human AE has been exploratively addressed by Wang et al (2013) and recently also by Pang et al (2014). Other studies on the immunopathology of AE revealed that CD4+CD25+ Treg cells play a critical role in human AE by blunting immune responses to specific antigens, or by suppressing the secretion of proinflammatory cytokines, especially through IL-10 and TGF-␤1 (Hübner et al, 2006).…”
Section: Biology and Immunology Of Susceptibility Versus Resistance Imentioning
confidence: 99%
“…The cellular programs are implemented, the inflammatory activation of immune-competent cells decreases, and the reparative processes due to the polarization of macrophages towards M2 phenotype are amplified [7, 8, 22, 26]. …”
Section: Resultsmentioning
confidence: 99%
“…Thus, the observed changes of the intracellular content of the factors such as CREB, AKT, SMAD, and p53 allow speaking about the possibility of switching cellular strategy from the implementation of proinflammatory responses to specific regulatory responses under the influence of the resonant microwaves at 1 GHz in the course of the activity reduction of stress-activated and mitogen-activated signaling pathways [6, 7, 22, 25, 35]. Recovery of normal cell reactivity will contribute to the realization of the effects CREB, aimed at improving the plasticity of the cells to specific signals, making the cell adapt to the new conditions.…”
Section: Resultsmentioning
confidence: 99%