From: The gut–liver axis in sepsis: interaction mechanisms and therapeutic potential
Location | Cell type | Function | Refs. |
---|---|---|---|
Mucous layer | Intestinal macrophages | Phagocytosis and degradation of microorganisms and dead tissue cells Producing mediators that drive epithelial cell renewal | [33] |
Dendritic cells | Having the ability to open TJs between epithelial cells and directly take up luminal microorganisms | [36] | |
Local interepithelial lymphocytes: conventional and nonconventional TCRαβ+ subsets; TCRγδ+ subgroups | Guarding the intestinal epithelial barrier Rapidly activating cytolytic and Th1-cell cytokine responses aimed at an infected or stressed epithelium | ||
ILC1 | Being activated by myeloid-cell-derived IL-12 | ||
ILC2 | Being activated by epithelial-derived cytokines and orchestrate type 2 immunity | ||
ILC3 | Interacting with cells of both the innate and adaptive immune systems Secreting IL-22 and initiating an antimicrobial program as well as barrier fortification in epithelial cells | ||
Intestinal B cells | Producing the SIgA | [40] | |
Invariant T cells: MAIT cells | Rapidly producing cytokines and exerting cytolytic activity after activation by cells infected with bacteria, including several enteric species | [34] | |
iNKT cells | Producing large amounts of IL-4 and IFN-γ involved in the immune response | [34] | |
Mucous layer and submucosa | Lymphatic follicles | Involved in the local immune response, namely through collaboration with epithelium to effectively localize entry of foreign materials to sites where antigens and microorganisms can be immediately endocytosed, processed, and presented for primary or memory immune responses without the need for systemic involvement | [31] |