CD4 T-Cell Subsets and the Pathophysiology of Inflammatory Bowel Disease.
Autor: Gómez Bris, Raquel; Saez Somolinos, Ángela; Herrero Fernández, Beatriz; Rius, Cristina; Sánchez-Martínez, Héctor; González-Granado, José M.
Resumen: Inflammatory bowel disease (IBD) is an umbrella term for the chronic immune-mediated
idiopathic inflammation of the gastrointestinal tract, manifesting as Crohn’s disease (CD) or ulcerative
colitis (UC). IBD is characterized by exacerbated innate and adaptive immunity in the gut in association
with microbiota dysbiosis and the disruption of the intestinal barrier, resulting in increased bacterial
exposure. In response to signals from microorganisms and damaged tissue, innate immune cells
produce inflammatory cytokines and factors that stimulate T and B cells of the adaptive immune
system, and a prominent characteristic of IBD patients is the accumulation of inflammatory T-cells
and their proinflammatory-associated cytokines in intestinal tissue. Upon antigen recognition and
activation, CD4 T-cells differentiate towards a range of distinct phenotypes: T helper(h)1, Th2, Th9,
Th17, Th22, T follicular helper (Tfh), and several types of T-regulatory cells (Treg). T-cells are generated
according to and adapt to microenvironmental conditions and participate in a complex network of
interactions among other immune cells that modulate the further progression of IBD. This review
examines the role of the CD4 T-cells most relevant to IBD, highlighting how these cells adapt to the
environment and interact with other cell populations to promote or inhibit the development of IBD.
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