Host FSTL1 defines the impact of stem cell therapy on liver fibrosis by potentiating the early recruitment of inflammatory macrophages.

Adult stem cell therapy holds great promise for treating decompensated liver cirrhosis on the basis of animal studies, despite uncertainty about its clinical therapeutic efficacy and unclear underlying mechanisms. Here, we investigated the role of follistatin-like 1 (FSTL1), a profibrotic and proinflammatory matricellular protein, in inflammation-related heterogeneity in stem cell therapy. Our results showed that a high level of circulating FSTL1 is significantly correlated with therapeutic response in patients with cirrhosis.

[Research progresses of Qa-1 restricted CD8 regulatory T cells in the pathogenesis of infectious diseases].

The Qa-1 in mice is homologous to human leukocyte antigen E(HLA-E), and both of them belong to the non-classical major histocompatibility complex I b(MHC-I b) molecules. Qa-1 is capable of presenting self or exogenous antigen peptides to interact with two distinct receptors, namely T cell receptor (TCR) and natural killer cell group 2 member A (or C) (NKG2A/C), thus playing an important role in immune response and regulation. Qa-1-restricted regulatory CD8 T cell (CD8 Treg) is one of the most studied CD8 Treg subgroups, which can maintain immune homeostasis and autoimmune tolerance by exerting immunosuppressive effects.

Alterations in CX3CL1 Levels and Its Role in Viral Pathogenesis.

CX3CL1, also named fractalkine or neurotactin, is the only known member of the CX3C chemokine family that can chemoattract several immune cells. CX3CL1 exists in both membrane-anchored and soluble forms, with each mediating distinct biological activities. CX3CL1 signals are transmitted through its unique receptor, CX3CR1, primarily expressed in the microglia of the central nervous system (CNS).

CD226 promotes renal fibrosis by regulating macrophage activation and migration.

It has been found that CD226 plays an important role in regulating macrophage function, but its expression and function in macrophages during renal fibrogenesis have not been studied. Our data demonstrated that CD226 expression in macrophages was obviously upregulated in the unilateral ureteral obstruction model, while CD226 deficiency attenuated collagen deposition in renal interstitium along with fewer M1 within renal cortex and renal medulla and a lower level of proinflammatory factors compared to that of control littermates. Further studies demonstrated that Cd226-/- bone marrow-derived macrophages transferring could significantly reduce the tubular injury, collagen deposition, and proinflammatory cytokine secretion compared with that of Cd226+/+ bone marrow-derived macrophages transferring in the unilateral ureteral obstruction model.

Innate lymphoid cell subsets in the pathogenesis of primary biliary cholangitis.

Background And Aim: Primary biliary cholangitis (PBC) is an autoimmune liver disease characterized by destructive lymphocytic cholangitis and specific anti-mitochondrial antibodies. Innate lymphoid cells (ILCs) have been reported to play a role in liver homeostasis and autoimmunity.

Methods: We evaluated the features of peripheral ILC1s and ILC3 in patients with PBC and hepatic ILC1 and ILC3 in two different PBC mouse models (dominant-negative transforming growth factor-beta receptor II [dnTGFβRII] and 2-octynoic acid-bovine serum albumin [2OA-BSA]).

[Advances in the role and mechanism of NK cell immune response mediated by NKG2A-HLA-E axis in viral infectious diseases].

Natural killer (NK) cells directly lysis the virus-infected cells through rapidly releasing cytotoxic mediators and cytokines. The balance between inhibitory and activated receptors on the surface of NK cells, as well as the corresponding ligands expressed on target cells are involved in the regulation of the cytotoxic function of NK cells. NKG2A is one of the highly anticipated inhibitory receptors expressed on NK cells, which can inhibit the cytotoxicity of NK cells to autologous normal tissue cells through interacting with the ligand HLA-E.

Ad5-nCoV Vaccination Could Induce HLA-E Restricted CD8 T Cell Responses Specific for Epitopes on Severe Acute Respiratory Syndrome Coronavirus 2 Spike Protein.

We evaluated cellular immune responses induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines in an immunized population based on HLA-E-restricted CD8 T cell epitope identification. HLA-E-restricted SARS-CoV-2 CD8 T cell nonamer peptides were predicted with software. An HLA-E-transfected K562 cell binding assay was used to screen for high-affinity peptides.

Erratum to "HLA-E-restricted Hantaan virus-specific CD8 T cell responses enhance the control of infection in hemorrhagic fever with renal syndrome" [Biosaf. Health 5 (2023) 289-299].

[This corrects the article DOI: 10.1016/j.bsheal.

CD226 maintains regulatory T cell phenotype stability and metabolism by the mTOR/Myc pathway under inflammatory conditions.

Regulatory T (Treg) cells exhibit immunosuppressive phenotypes and particular metabolic patterns with certain degrees of plasticity. Previous studies of the effects of the co-stimulatory molecule CD226 on Treg cells are controversial. Here, we show that CD226 primarily maintains the Treg cell stability and metabolism phenotype under inflammatory conditions.

Increased blood CD226 inflammatory monocytes with low antigen presenting potential correlate positively with severity of hemorrhagic fever with renal syndrome.

Background: Hantaan virus (HTNV) infection can cause severe hemorrhagic fever with renal syndrome (HFRS). Inflammatory monocytes (iMOs) are involved in early antiviral responses. Previous studies have found that blood iMOs numbers increase in the acute phase of HFRS.

HLA-E-restricted Hantaan virus-specific CD8 T cell responses enhance the control of infection in hemorrhagic fever with renal syndrome.

Infection with the Hantaan virus (HTNV) may result in severe hemorrhagic fever with renal syndrome (HFRS). The functions of HLA-E-restricted CD8 T lymphocytes in virus control and vaccine development have recently received increased attention. The purpose of this research is to discover HLA-E-restricted CD8 T cell epitopes on HTNV as well as the features of these epitope-specific CD8 T cells in HFRS patients.

IL-15 induced bystander activation of CD8 T cells may mediate endothelium injury through NKG2D in Hantaan virus infection.

Introduction: Hantaan virus (HTNV) can cause endothelium injury in hemorrhagic fever with renal syndrome (HFRS) patients. Bystander activation of CD8+ T cells by virus infection has been shown that was involved in host injury, but it is unclear during HTNV infection. This project aimed to study the effect of bystander-activated CD8+ T cell responses in HTNV infection.

HTNV infection induces activation and deficiency of CD8+MAIT cells in HFRS patients.

Hantaan virus (HTNV) infection causes an epidemic of hemorrhagic fever with renal syndrome (HFRS) mainly in Asia. Mucosal-associated invariant T (MAIT) cells are innate-like T lymphocytes known to play an important role in innate host defense during virus infection. However, their roles and phenotypes during HTNV infection have not yet been explored.

Hantaan virus-induced elevation of plasma osteoprotegerin and its clinical implications in hemorrhagic fever with renal syndrome.

Objectives: The bleeding tendency is a hallmark of hemorrhagic fever with renal syndrome (HFRS) after Hantaan virus (HTNV) infection. Growing reports indicate the importance of osteoprotegerin (OPG) in vascular homeostasis, implying OPG might be involved in the pathogenesis of coagulopathy in patients with HFRS.

Methods: Acute and convalescence plasmas of 32 patients with HFRS were collected.

[The role of red blood cells in immune response to infection: A review].

Red blood cells are the largest number of cells in blood. Apart from transporting oxygen and carbon dioxide, they also regulate the immune responses. It has been confirmed that red blood cells can play a role in clearing immune complex, promoting phagocytosis, and presenting antigen through immune adhesion.

Anti-platelet factor 4/heparin antibodies in patients with Hantaan virus infection.

Background: Hemorrhagic fever with renal syndrome (HFRS) induced by Hantaan virus infection and heparin-induced thrombocytopenia (HIT) are associated with symptoms such as thrombocytopenia and thrombosis. However, related molecules, such as anti-platelet factor 4 (PF4)/heparin antibodies, in patients with HFRS have not been evaluated.

Objectives: To test plasma levels of anti-PF4/heparin antibodies and study the possible role of these antibodies in HFRS pathogenesis.

Endogenous Follistatin-like 1 guarantees the immunomodulatory properties of mesenchymal stem cells during liver fibrotic therapy.

Background: Mesenchymal stem cell (MSC) therapy has been shown to be a promising option for liver fibrosis treatment. However, critical factors affecting the efficacy of MSC therapy for liver fibrosis remain unknown. Follistatin-like 1 (FSTL1), a TGF-β-induced matricellular protein, is documented as an intrinsic regulator of proliferation and differentiation in MSCs.

Expression of CD226 is upregulated on Tr1 cells from neuromyelitis optica spectrum disorder patients.

Background: Neuromyelitis optica spectrum disorder (NMOSD) is a central and acute demyelinating disease of the central nervous system with unusual clinical course. The development of novel biomarkers for NMOSD is critical for implementing effective clinical treatment. CD226 is known to be expressed on many types of peripheral lymphoid cells.

CD226 knockout alleviates high-fat diet induced obesity by suppressing proinflammatory macrophage phenotype.

Obesity is associated with chronic low-grade inflammation, contributing to an increasing prevalence of chronic metabolic diseases, such as insulin resistance, non-alcoholic fatty liver disease (NALFD), and steatohepatitis. Macrophages are the predominant immune cells in adipose tissues. Adipose tissue macrophages (ATMs) would switch to pro-inflammatory M1 state during obesity, causing local and systemic inflammation.

[Preparation and identification of mouse-derived monoclonal antibodies to human ST2 molecule].

Objective To prepare mouse-derived monoclonal antibody against human suppression of tumorigenicity 2 (ST2) molecule and make initial identification. Methods BALB/c mice were immunized with the recombinant human ST2 molecule, and the conventional B-cell hybridoma technology was used to prepare the anti-ST2 monoclonal antibodies (mAbs). Their application in western blotting, immunohistochemistry, and flow cytometry were evaluated.

CD226 deficiency promotes glutaminolysis and alleviates mitochondria damage in vascular endothelial cells under hemorrhagic shock.

Hemorrhagic shock (HS) is common in clinical emergencies, leading to millions of deaths each year globally. CD226 is a costimulatory adhesion molecule expressed on both immune cells and endothelial cells (ECs) to regulate their metabolic activity and function. As endothelial dysfunction occurs after HS, the roles CD226 plays in vascular EC metabolism were investigated.

GDF15 induces immunosuppression via CD48 on regulatory T cells in hepatocellular carcinoma.

Background: A better understanding of the molecular mechanisms that manifest in the immunosuppressive tumor microenvironment (TME) is crucial for developing more efficacious immunotherapies for hepatocellular carcinoma (HCC), which has a poor response to current immunotherapies. Regulatory T (Treg) cells are key mediators of HCC-associated immunosuppression. We investigated the selective mechanism exploited by HCC that lead to Treg cells expansion and to find more efficacious immunotherapies.