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The gut-immune axis, specifically the interaction between dendritic cells (DCs) and T cells, is a fundamental component of mucosal immunity and intestinal homeostasis [1]. Dendritic cells in the lamina propria and mesenteric lymph nodes sample luminal antigens and present them to naive T cells, determining the balance between immune tolerance and active immunity [2]. This process involves the induction of regulatory T cells (Tregs) to maintain tolerance to commensal bacteria or the activation of effector T cells (Th1, Th17) to combat pathogens [3]. Dysregulation of this axis is a primary driver of chronic inflammatory conditions such as Inflammatory Bowel Disease (IBD), where an overactive immune response leads to persistent tissue damage [4]. While not a single molecular target, this axis is the focus of numerous therapeutic interventions that target specific receptors and cytokines involved in cell trafficking and signaling, such as integrin alpha-4 beta-7 and the IL-12/IL-23 pathway [5]. Drugs like vedolizumab and ustekinumab modulate this axis to restore homeostasis in patients with Crohn's disease and ulcerative colitis [6]. Sources: [1] Coombes, J. L., & Powrie, F. (2008). Nature Reviews Immunology, 8(6), 435-446. [2] Belkaid, Y., & Hand, T. W. (2014). Cell, 157(1), 121-141. [3] Sun, M., et al. (2020). Frontiers in Immunology, 11, 598. [4] Neurath, M. F. (2017). Nature Reviews Gastroenterology & Hepatology, 14(5), 283-295. [5] Sands, B. E., et al. (2019). New England Journal of Medicine, 381(13), 1201-1214. [6] Mowat, A. M. (2003). Nature Reviews Immunology, 3(4), 331-341.
Modulation of lymphocyte trafficking to the gut mucosa and inhibition of pro-inflammatory cytokine signaling between dendritic cells and T cells.
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