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Table 1 Gut immune cells in the intestinal wall

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

[34, 35]

ILC1

Being activated by myeloid-cell-derived IL-12

[37, 38]

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]

  1. IFN, interferon; IL, interleukin; ILC, innate lymphoid cell; iNKT, invariant natural killer T; MAIT, mucosal-associated invariant T; TCRαβ+, αβ T cell receptor+; TCRγδ+, γδ T cell receptor+; Th1, T helper 1; TJs, tight junctions; SIgA, secretory immunoglobulin A