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Yang, K., Shrestha, S., Zeng, H., Karmaus, P.W., Neale, G., Vogel, P., et al. (2013) T Cell Exit from Quiescence and Differentiation into Th2 Cells Depend on Raptor-MTORC1-Mediated Metabolic Reprogramming. Immunity, 39, 1043-1056.
https://doi.org/10.1016/j.immuni.2013.09.015

has been cited by the following article:

• TITLE: Clostridium difficile Toxin B: Insights into Its Target Genes

  AUTHORS: Junyi Hu, Yunjie Shan, Huan Yang

  KEYWORDS: Clostridium difficile Infection, TcdB, Gene Regulation

  JOURNAL NAME: Open Journal of Applied Sciences, Vol.12 No.3, March 24, 2022

  ABSTRACT: Clostridium difficile is a grossly Gram-positive anaerobic bacterium that has been a key factor in inducing imbalances in the gut microbiota in recent years, leading to intestinal-associated inflammation. The main pathogenic toxins of Clostridium difficile are toxin A (TcdA) and toxin B (TcdB). TcdB is the main pathogenic factor of Clostridium difficile infection. This review revealed the pathogenic mechanism of Clostridium difficile toxin B, expounded the impact of Clostridium difficile on the intestinal system, and predicted the genes on which TcdB may act, thereby providing a new therapeutic target for Clostridium difficile infection, offering theoretical basis and new strategies for clinical prevention and control.