Pathophysiology of Inflammatory Bowel Disease: Innate Immune System.
Autor: Saez Somolinos, Ángela; Herrero-Fernandez, Beatriz; Gómez Bris, Raquel; Sánchez-Martínez, Héctor; González Granado, José M.
Resumen: Abstract: Inflammatory bowel disease (IBD), comprising Crohn’s disease (CD) and ulcerative colitis
(UC), is a heterogeneous state of chronic intestinal inflammation with no exact known cause. Intestinal
innate immunity is enacted by neutrophils, monocytes, macrophages, and dendritic cells (DCs),
and innate lymphoid cells and NK cells, characterized by their capacity to produce a rapid and
nonspecific reaction as a first-line response. Innate immune cells (IIC) defend against pathogens and
excessive entry of intestinal microorganisms, while preserving immune tolerance to resident intestinal
microbiota. Changes to this equilibrium are linked to intestinal inflammation in the gut and IBD.
IICs mediate host defense responses, inflammation, and tissue healing by producing cytokines and
chemokines, activating the complement cascade and phagocytosis, or presenting antigens to activate
the adaptive immune response. IICs exert important functions that promote or ameliorate the cellular
and molecular mechanisms that underlie and sustain IBD. A comprehensive understanding of the
mechanisms underlying these clinical manifestations will be important for developing therapies
targeting the innate immune system in IBD patients. This review examines the complex roles of
and interactions among IICs, and their interactions with other immune and non-immune cells in
homeostasis and pathological conditions.
Ficheros en el ítem
Ficheros | Tamaño | Formato | Ver |
---|---|---|---|
ijms-24-01526-v2.pdf | 2.797Mb | Ver/ |
Este ítem aparece en la(s) siguiente(s) colección(ones)
- CIENCIAS EXPERIMENTALES [319]