Roles of hepatic immunity in metabolic dysfunction-associated steatotic liver disease: Cellular and molecular mechanisms and clinical trials

Table 1 Roles of different innate immune cells in the progression of metabolic dysfunction-associated steatotic liver disease

Cells	Markers	Functions	Ref.
cDCs	CD103	Adoptive transfer of CD103-expressing cDCs protected liver inflammation and damage in Batf3-deficient animals with a high sucrose diet or MCD diet during MASH progression	Heier et al[15]
cDCs	XCR1+	XCR1+ cDC1 cells influence inflammatory T cell reprogramming and exacerbate MASH development	Deczkowska et al[16]
Macrophages	MERTK	Ablation of MERTK signaling by disintegrin and metalloproteinase domain-containing protein 17 decreased MASH progression	Cai et al[23]
Macrophages	Ly6C+OPN+	Infiltration of Ly6C+OPN+ lipid-associated macrophages promoted MASH progression	Kui et al[38]
Neutrophils	Ly6G+H3Cit+	Infiltration of Ly6G+H3Cit+ neutrophils promoted MASH progression	Kui et al[38]
NK cells	CXCR3+	CXCR3+ NK cells decreased liver inflammation in MCD-induced MASH in mice	Fan et al[44]
NKT cells	IL-17A+	IL-17A-expressing invariant NKT cells in peripheral blood mononuclear cells were associated with MASH progression in patients	Maricic et al[51]
MAIT cells	TCRVa7.2+ CD161high CD3+	The frequency of MAIT cells in circulating blood in patients with MASH decreased compared to that in the group with steatosis or healthy controls	Waller et al[52]
ILCs	CD45+ TCRβ- B220-; NK1.1+ CD49a+ CD49b-	Increasing the frequency of ILC1 frequency by fecal microbiota transplantation and indole-3-carbinol inhibited MASLD	Hou et al[58]

cDCs: Conventional dendritic cells; ILC: Innate lymphoid cell; MAIT: Mucosal-associated invariant T; NK: Natural killer cell; NKT: Natural killer T cell; TCR: T cell receptor; CD: Cluster of differentiation; IL: Interleukin; MCD: Methionine- and choline-deficient; MASH: Metabolic dysfunction-associated steatohepatitis; XCR: X-C motif chemokine receptor; CXCR: C-X-C motif chemokine receptor.