Differential expression of HLA-G and ILT-2 receptor in human tuberculosis: Localized versus disseminated disease

Saurabh, Abhinav; Thakral, Deepshi; Mourya, Manish; Singh, Amar; Bhatnagar, Anuj; Mitra, Dipendra Kumar; Kanga, Uma

doi:10.1016/j.humimm.2016.01.004

Cited by 5 publications

(1 citation statement)

References 51 publications

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“…CD14 + monocytes constitute the main subset of immune cells expressing HLA-G, although at low and variable levels [e.g., 0.12% ± 0.07% of HLA-G + CD14 + cells (20)(21)(22)(23)(24)]. In our cohort of HCs, circulating DC-10 expressed significantly higher HLA-G levels compared to those expressed by total CD14 + cells in terms of both percentage of HLA-G + cells (2.19% ± 3.84% and 0.66% ± 0.93%, respectively, p < 0.0001) and levels of protein expression (MFI of HLA-G, 25.95% ± 10.82% and 26.23% ± 18.96%, respectively, p < 0.0001) (Figure 2B and Supplementary Figure S2A).…”

Section: Dc-10 Contain a Higher Proportion Of Hla-g-expressing Cells Than Do Total Cd14 + Cells Cd11c + Cells And Cdc1mentioning

confidence: 99%

Altered Frequency and Phenotype of HLA-G-Expressing DC-10 in Type 1 Diabetes Patients at Onset and in Subjects at Risk to Develop the Disease

et al. 2021

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Type 1 diabetes (T1D) is a chronic autoimmune disease resulting in progressive destruction of β-cells. Several factors affecting lymphocyte and antigen-presenting cells, including dendritic cells (DCs), contribute to defective maintenance of tolerance in T1D. DC-10 are a subset of human DCs involved in IL-10-mediated tolerance. A precise monitoring of DC-10 in the peripheral blood is possible thanks to the discovery of specific biomarkers. DC-10, being cells that naturally express HLA-G, may be used for the appropriate staging of the disease. By enumerating and phenotypically characterizing DC-10 in the peripheral blood of subjects at different stages of T1D development—first-degree relatives (FDRs) of T1D patients, without (Abneg) or with (Abpos) autoantibodies, T1D patients at onset, and age-matched healthy controls (HCs)—we showed that DC-10 contain a high proportion of HLA-G-expressing cells as compared with monocytes. We reported that a low frequency of DC-10 during disease development is paralleled with the increased proportion of pro-inflammatory cDC2 cells. Moreover, DC-10 number and phenotype differ from Abneg FDRs, Abpos FDRs, and T1D patients compared with HCs, and DC-10 from T1D patients express low levels of CD83. Finally, multiple regression analysis, considering DC-10 and HLA-G-related parameters, showed that Abneg FDRs are more similar to subjects with autoimmunity than to HCs. This is the first demonstration that impairment in DC-10 number and phenotype, specifically CD83 expression, is associated with risk of developing T1D, suggesting a possible use of CD83+ DC-10 to stratify individuals at risk of T1D in conjunction with classical prognostic factors.

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Section: Dc-10 Contain a Higher Proportion Of Hla-g-expressing Cells Than Do Total Cd14 + Cells Cd11c + Cells And Cdc1mentioning

confidence: 99%

Altered Frequency and Phenotype of HLA-G-Expressing DC-10 in Type 1 Diabetes Patients at Onset and in Subjects at Risk to Develop the Disease

et al. 2021

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Inhibiting HLA-G restores IFN-γ and TNF-α producing T cell in pleural Tuberculosis

et al. 2018

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LILRB1-HLA-G axis defines a checkpoint driving natural killer cell exhaustion in tuberculosis

Wang,

Chai,

Lei

et al. 2024

EMBO Mol Med

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Chronic infections, including Mycobacterium tuberculosis (Mtb)-caused tuberculosis (TB), can induce host immune exhaustion. However, the key checkpoint molecules involved in this process and the underlying regulatory mechanisms remain largely undefined, which impede the application of checkpoint-based immunotherapy in infectious diseases. Here, through adopting time-of-flight mass cytometry and transcriptional profiling to systematically analyze natural killer (NK) cell surface receptors, we identify leukocyte immunoglobulin like receptor B1 (LILRB1) as a critical checkpoint receptor that defines a TB-associated cell subset (LILRB1+ NK cells) and drives NK cell exhaustion in TB. Mechanistically, Mtb-infected macrophages display high expression of human leukocyte antigen-G (HLA-G), which upregulates and activates LILRB1 on NK cells to impair their functions by inhibiting mitogen-activated protein kinase (MAPK) signaling via tyrosine phosphatases SHP1/2. Furthermore, LILRB1 blockade restores NK cell-dependent anti-Mtb immunity in immuno-humanized mice. Thus, LILRB1-HLA-G axis constitutes a NK cell immune checkpoint in TB and serves as a promising immunotherapy target.

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Differential expression of HLA-G and ILT-2 receptor in human tuberculosis: Localized versus disseminated disease

Cited by 5 publications

References 51 publications

Altered Frequency and Phenotype of HLA-G-Expressing DC-10 in Type 1 Diabetes Patients at Onset and in Subjects at Risk to Develop the Disease

Altered Frequency and Phenotype of HLA-G-Expressing DC-10 in Type 1 Diabetes Patients at Onset and in Subjects at Risk to Develop the Disease

Inhibiting HLA-G restores IFN-γ and TNF-α producing T cell in pleural Tuberculosis

LILRB1-HLA-G axis defines a checkpoint driving natural killer cell exhaustion in tuberculosis

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