Although macrophages (Mϕ) maintain intestinal immune homoeostasis, there is not much available information about their subset composition, phenotype and function in the human setting. Human intestinal Mϕ (CD45⁺HLA-DR⁺CD14⁺CD64⁺) can be divided into subsets based on the expression of CD11c, CCR2 and CX3CR1. Monocyte-like cells can be identified as CD11c^highCCR2⁺CX3CR1⁺ cells, a phenotype also shared by circulating CD14⁺ monocytes. On the contrary, their Mϕ-like tissue-resident counterparts display a CD11c^-CCR2^-CX3CR1^- phenotype. CD11c^high monocyte-like cells produced IL-1β, both in resting conditions and after LPS stimulation, while CD11c^- Mϕ-like cells produced IL-10. CD11c^high pro-inflammatory monocyte-like cells, but not the others, were increased in the inflamed colon from patients with inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis. Tolerogenic IL-10-producing CD11c^- Mϕ-like cells were generated from monocytes following mucosal conditioning. Finally, the colonic mucosa recruited circulating CD14⁺ monocytes in a CCR2-dependent manner, being such capacity expanded in IBD. Mϕ subsets represent, therefore, transition stages from newly arrived pro-inflammatory monocyte-like cells (CD11c^highCCR2⁺CX3CR1⁺) into tolerogenic tissue-resident (CD11c^-CCR2^-CX3CR1^-) Mϕ-like cells as reflected by the mucosal capacity to recruit circulating monocytes and induce CD11c^- Mϕ. The process is nevertheless dysregulated in IBD, where there is an increased migration and accumulation of pro-inflammatory CD11c^high monocyte-like cells.

中文翻译：

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人肠道促炎性 CD11chighCCR2+CX3CR1+ 巨噬细胞，而不是它们的致耐受性 CD11c-CCR2-CX3CR1- 对应物，在炎症性肠病中扩增。

尽管巨噬细胞 (Mϕ) 维持肠道免疫稳态，但关于它们在人类环境中的亚群组成、表型和功能的可用信息并不多。人肠道 Mφ (CD45 ⁺ HLA-DR ⁺ CD14 ⁺ CD64 ⁺ ) 可根据 CD11c、CCR2 和 CX3CR1 的表达分为亚群。单核细胞样细胞可被鉴定为 CD11c^高CCR2 ⁺ CX3CR1 ⁺细胞，循环 CD14 ⁺单核细胞也具有这种表型。相反，它们的 Mφ 样组织驻留对应物显示 CD11c ^- CCR2 ^- CX3CR1 ^-表型。CD11c^高单核细胞样细胞在静息条件下和 LPS 刺激后均产生 IL-1β，而 CD11c ^- Mφ 样细胞产生 IL-10。CD11c^高促炎性单核细胞样细胞在炎症性肠病 (IBD)（包括克罗恩病和溃疡性结肠炎）患者的发炎结肠中增加，但其他细胞没有。在粘膜调节后，产生致耐受性 IL-10 的 CD11c ^- Mφ 样细胞从单核细胞中产生。最后，结肠粘膜以 CCR2 依赖性方式募集循环 CD14 ^{+单核细胞，这种能力在 IBD 中得到了扩展。}因此，Mϕ 子集代表新到达的促炎性单核细胞样细胞（CD11c^高CCR2⁺ CX3CR1 ⁺ ) 进入致耐受性组织驻留 (CD11c ^- CCR2 ^- CX3CR1 ^- ) Mϕ 样​​细胞，这反映在粘膜招募循环单核细胞和诱导 CD11c ^- Mϕ 的能力上。尽管如此，该过程在 IBD 中失调，其中促炎性 CD11c^高单核细胞样细胞的迁移和积累增加。