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Review
. 2023 Feb 9:14:1138971.
doi: 10.3389/fimmu.2023.1138971. eCollection 2023.

Immunoregulation by antigen-presenting cells in human intestinal lamina propria

Affiliations
Review

Immunoregulation by antigen-presenting cells in human intestinal lamina propria

Takayuki Ogino et al. Front Immunol. .

Abstract

Antigen-presenting cells, including macrophages and dendritic cells, are a type of innate immune cells that can induce the differentiation of T cells and activate the adaptive immune response. In recent years, diverse subsets of macrophages and dendritic cells have been identified in the intestinal lamina propria of mice and humans. These subsets contribute to the maintenance of intestinal tissue homeostasis by regulating the adaptive immune system and epithelial barrier function through interaction with intestinal bacteria. Further investigation of the roles of antigen-presenting cells localized in the intestinal tract may lead to the elucidation of inflammatory bowel disease pathology and the development of novel treatment approaches.

Keywords: antigen-presenting cell; dendritic cell; helper T cell; inflammatory bowel disease; macrophage; mucosal immunology.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
The difference of immunoregulation between steady state and IBD. In human intestinal lamina propria, CD14+CD163low cells induce Th17 differentiation in an IL-6, IL-23p19, TNF-α, and IL-1β dependent manner. CD14+CD163highCD160high cells suppress the proliferation of CD4+ T cells. CD103+ dendritic cells induce Treg cells in steady-state (left). On the other hand, in Crohn’s disease, CD14+CD163low cells have significantly increased expression of IL-6, IL-23p19, and TNF-α, as well as enhanced Th17 induction capacity. In ulcerative colitis, CD14+CD163highCD160high cells reduce the ability to suppress CD4+ T cell proliferation, and CD103+ dendritic cells showed reduced Treg- and enhanced Th17-inducing capacity (right).

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