Table 2.
Changes in immune cells in obese individual
| Cell | Tendency | Mechanism | References |
|---|---|---|---|
| uNKs | down | Obesity leads to a significant decrease in the number of uNK cells, accompanied by impaired uterine artery remodeling. In addition, the exaggerated response of uNK cells to PDGF in obesity results in the overexpression of decorin, which restricts trophoblast survival and significantly inhibits placental development. This suggests that obesity-induced alterations in utero-resident immune cells severely impede placental development. | [70] |
| Adipose tissue NK cells | up | Human adipose tissue NK cells express higher levels of activation markers compared to peripheral blood NK cells. Adipose tissue NK cells also exhibit an activated phenotype in obese individuals compared to lean subjects, showing elevated expression of the activating receptor NKG2D. | [71] |
| NK cells | / | Maternal obesity resulting from a high-fat, high-sugar diet may decrease IFN-γ expression in NK cells, potentially impairing angiogenesis in early pregnancy. | [72] |
| Macrophages | up | Proinflammatory macrophages accumulation is a central feature of obesity and a major component of fat inflammation associated with obesity complications. | [67] |
| M1 macrophages | down | Compared with control women, women with obesity had lower levels of M1 (HLA-DR+CD163−) macrophages and higher levels of M2 (HLA-DR−CD163) macrophages in the decidua of the parietalis, and these lower levels of M1 macrophages in women with obesity may represent a compensatory mechanism to compensate for the increased pro-inflammatory state associated with obesity. | [73] |
| Decidual macrophages | up | An increased influx of macrophages and overexpression of IL-6 and GRO-α in the placenta of women with obesity lead to excessive inflammation, raising the risk of pregnancy complications. | [74] |
| HBCs | up | Maternal obesity and fetal sex significantly affect the density of CD163 + HBC in the placental villi, leading to an increase in their number and pro-inflammatory phenotype. | [75] |
| Adipose tissue macrophages | up | Macrophages produce IL-1β, which enhances the release of IL-17 and IL-22 by adipose tissue CD4 + T cells. IL-22, in turn, upregulates the transcription of pro-IL-1β, leading to an enhancement in the production of IL-1β by adipose tissue macrophages. Formation of a feedforward pro-inflammatory loop between macrophages and CD4 + T cells contributes to a significant pro-inflammatory signature of adipose tissue macrophages in patients with obesity and type 2 diabetes. | [76] |
| T cells | up | Th1-type immunity is predominant in systemic immunization of PCOS patients. Th1/Th2 immune imbalance is associated with obesity, particularly abdominal obesity. | [77] |
| adipose-tissue-resident T cells | / | In obese mice, the cell balance changed: there were more CD8 + T cells than Th1 CD4 + T cells, fewer regulatory T cells, and a predominance of pro-inflammatory macrophages. These effector cells promote inflammation and worsen adipose tissue dysfunction by producing inflammatory cytokines. | [78] |
| ATDCs | up | Immature ATDCs are a crucial cell type whose production is elevated in obese adipose tissue compared to lean controls. Increased ATDCs can stimulate the generation of pro-inflammatory Th17 cells, which, in turn, play a significant role in inflammation in obese adipose tissue. | [79] |
| ATDCs | up | When fed a moderately HFD, ATDCs constituted the majority of the CD11c + cell population induced by adipose tissue. Ccr7−/− mice, with decreased ATDC content, were shielded from insulin resistance, which is a significant factor in obesity-induced adipose tissue inflammation. | [80] |
| DCs | up | Obesity is similar to aging, leading to elevated serum levels of pro-inflammatory cytokines and autoimmune antibodies. B cells from obese adults and older adults can also secrete inflammatory cytokines and promote the generation of inflammatory T cells. The pro-inflammatory characteristics of B cells from obese individuals were significantly diminished by weight loss, but not completely reversed. | [81] |
| B cells | up | [82] |
/ not specified, uNKs uterine NK cells, HBCs hofbauer cells, ATDCs adipose tissue dendritic cells, DCs dendritic cells, PDGF platelet derived growth factor, NKG2D natural killer group 2 member D, IFN-γ interferon-γ, IL-6 interleukin-6, GRO-α growth-regulatedonco-gene-alpha, IL-1β interleukin-1β, PCOS polycystic ovary syndrome