MHC Class I Recognition by Monocyte-/Macrophage-Specific Receptors

Yoshida, Ryotaro

doi:10.1016/b978-0-12-800147-9.00007-8

Cited by 14 publications

(8 citation statements)

References 81 publications

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“…By contrast, four inhibitors, HIVEP2 (72), NKIRAS1 (73), NLK (74) and NKRF (75) of the canonical NFKB signaling pathway were expressed 2.8 to 11.8-fold higher in carriers than in non-carriers. Additionally, two immune inhibitory microRNAs, MIR221 (77,78) and MIR503HG (79) as well as one proinflammatory one, MIR155, which also has both anti-apoptotic activity (115,116) and an inhibitory effect on interferon signaling (76), were upregulated TABLE 3 | Mean expression levels (microarray signal intensity, MSI), false discovery rates (FDR) and fold differences (+ and -values as up-and down-regulated in carriers compared to non-carriers, respectively) of differentially expressed genes supporting decreased numbers of neutrophils, antigen-experienced T cells and dendritic cells and increased number of naïve and natural intraepithelial lymphocytes. resident immune cells such as IEL.…”

Section: Signal Transducing Genesmentioning

confidence: 99%

Mechanisms of Maintenance of Foot-and-Mouth Disease Virus Persistence Inferred From Genes Differentially Expressed in Nasopharyngeal Epithelia of Virus Carriers and Non-carriers

et al. 2020

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Foot-and-mouth disease virus (FMDV) causes persistent infection of nasopharyngeal epithelial cells in ∼50% of infected ruminants. The mechanisms involved are not clear. This study provides a continued investigation of differentially expressed genes (DEG) identified in a previously published transcriptomic study analyzing micro-dissected epithelial samples from FMDV carriers and non-carriers. Pathway analysis of DEG indicated that immune cell trafficking, cell death and hematological system could be affected by the differential gene expression. Further examination of the DEG identified five downregulated (chemerin, CCL23, CXCL15, CXCL16, and CXCL17) and one upregulated (CCL2) chemokines in carriers compared to non-carriers. The differential expression could reduce the recruitment of neutrophils, antigen-experienced T cells and dendritic cells and increase the migration of macrophages and NK cells to the epithelia in carriers, which was supported by DEG expressed in these immune cells. Downregulated chemokine expression could be mainly due to the inhibition of canonical NFκB signaling based on DEG in the signaling pathways and transcription factor binding sites predicted from the proximal promoters. Additionally, upregulated CD69, IL33, and NID1 and downregulated CASP3, IL17RA, NCR3LG1, TP53BP1, TRAF3, and TRAF6 in carriers could inhibit the Th17 response, NK cell cytotoxicity and apoptosis. Based on our findings, we hypothesize that (1) under-expression of chemokines that recruit neutrophils, antigen-experienced T cells and dendritic cells, (2) blocking NK cell binding to target cells and (3) suppression of apoptosis induced by death receptor signaling, viral RNA, and cell-mediated cytotoxicity in the epithelia compromised virus clearance and allowed FMDV to persist. These hypothesized mechanisms provide novel information for further investigation of persistent FMDV infection.

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Section: Signal Transducing Genesmentioning

confidence: 99%

Mechanisms of Maintenance of Foot-and-Mouth Disease Virus Persistence Inferred From Genes Differentially Expressed in Nasopharyngeal Epithelia of Virus Carriers and Non-carriers

et al. 2020

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“…Mϕ and dendritic cells (DCs) are phagocytic professional antigen presenting cells (APC) of myeloid lineage that are integral to the propagation and orchestration of immune responses. Although DCs are the main myeloid cell (MC) population responsible for antigen presentation, phagocytosed antigens are also processed by Mϕ and presented on the Mϕ surface by MHC-I and–II molecules to activate both B cells [2] and T cells [3–5].…”

Section: Introductionmentioning

confidence: 99%

Identification of alterations in macrophage activation associated with disease activity in systemic lupus erythematosus

et al. 2018

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Systemic lupus erythematosus (SLE) is characterized by abnormalities in B cell and T cell function, but the role of disturbances in the activation status of macrophages (Mϕ) has not been well described in human patients. To address this, gene expression profiles from isolated lymphoid and myeloid populations were analyzed to identify differentially expressed (DE) genes between healthy controls and patients with either inactive or active SLE. While hundreds of DE genes were identified in B and T cells of active SLE patients, there were no DE genes found in B or T cells from patients with inactive SLE compared to healthy controls. In contrast, large numbers of DE genes were found in myeloid cells (MC) from both active and inactive SLE patients. Among the DE genes were several known to play roles in Mϕ activation and polarization, including the M1 genes STAT1 and SOCS3 and the M2 genes STAT3, STAT6, and CD163. M1-associated genes were far more frequent in data sets from active versus inactive SLE patients. To characterize the relationship between Mϕ activation and disease activity in greater detail, weighted gene co-expression network analysis (WGCNA) was used to identify modules of genes associated with clinical activity in SLE patients. Among these were disease activity-correlated modules containing activation signatures of predominantly M1-associated genes. No disease activity-correlated modules were enriched in M2-associated genes. Pathway and upstream regulator analysis of DE genes from both active and inactive SLE MC were cross-referenced with high-scoring hits from the drug discovery Library of Integrated Network-based Cellular Signatures (LINCS) to identify new strategies to treat both stages of SLE. A machine learning approach employing MC gene modules and a generalized linear model was able to predict the disease activity status in unrelated gene expression data sets. In summary, altered MC gene expression is characteristic of both active and inactive SLE. However, disease activity is associated with an alteration in the activation of MC, with a bias toward the M1 proinflammatory phenotype. These data suggest that while hyperactivity of B cells and T cells is associated with active SLE, MC potentially direct flare-ups and remission by altering their activation status toward the M1 state.

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“…EMR1 mediates the induction of antigen-specific efferent regulatory T cells in peripheral tolerance [ 125 ]. MFSD6 is a mediator of MHC haplotype-dependent but not MHC-unrestricted cytotoxicity of macrophages [ 126 ]. SIGLEC11 and SIGLEC15 are mainly expressed on macrophages and have an immunosuppressive effect on macrophages [ 48 , 127 ].…”

Section: Resultsmentioning

confidence: 99%

Inferred Causal Mechanisms of Persistent FMDV Infection in Cattle from Differential Gene Expression in the Nasopharyngeal Mucosa

et al. 2022

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Foot-and-mouth disease virus (FMDV) can persistently infect pharyngeal epithelia in ruminants but not in pigs. Our previous studies demonstrated that persistent FMDV infection in cattle was associated with under-expression of several chemokines that recruit immune cells. This report focuses on the analysis of differentially expressed genes (DEG) identified during the transitional phase of infection, defined as the period when animals diverge between becoming carriers or terminators. During this phase, Th17-stimulating cytokines (IL6 and IL23A) and Th17-recruiting chemokines (CCL14 and CCL20) were upregulated in animals that were still infected (transitional carriers) compared to those that had recently cleared infection (terminators), whereas chemokines recruiting neutrophils and CD8+ T effector cells (CCL3 and ELR+CXCLs) were downregulated. Upregulated Th17-specific receptor, CCR6, and Th17-associated genes, CD146, MIR155, and ThPOK, suggested increased Th17 cell activity in transitional carriers. However, a complex interplay of the Th17 regulatory axis was indicated by non-significant upregulation of IL17A and downregulation of IL17F, two hallmarks of TH17 activity. Other DEG suggested that transitional carriers had upregulated aryl hydrocarbon receptor (AHR), non-canonical NFκB signaling, and downregulated canonical NFκB signaling. The results described herein provide novel insights into the mechanisms of establishment of FMDV persistence. Additionally, the fact that ruminants, unlike pigs, produce a large amount of AHR ligands suggests a plausible explanation of why FMDV persists in ruminants, but not in pigs.

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MHC Class I Recognition by Monocyte-/Macrophage-Specific Receptors

Cited by 14 publications

References 81 publications

Mechanisms of Maintenance of Foot-and-Mouth Disease Virus Persistence Inferred From Genes Differentially Expressed in Nasopharyngeal Epithelia of Virus Carriers and Non-carriers

Mechanisms of Maintenance of Foot-and-Mouth Disease Virus Persistence Inferred From Genes Differentially Expressed in Nasopharyngeal Epithelia of Virus Carriers and Non-carriers

Identification of alterations in macrophage activation associated with disease activity in systemic lupus erythematosus

Inferred Causal Mechanisms of Persistent FMDV Infection in Cattle from Differential Gene Expression in the Nasopharyngeal Mucosa

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