Chronic stress suppresses the immune system and especially the metabolism of components in the cytotoxic system, and the proliferation and maturation of cells essential for the body's protection against disease agents. This may be the reason for the increase in morbidity in chronic stressful situations.

At the early stage of mycoplasma respiratory infection, IL-17 can be protective as it can induce epithelial cell activation-secreting chemokines to recruit neutrophils for host defence, producing antimicrobial peptides to maintain the lung barrier function; however, aberrant release of IL-17 in the lung results in persistent neutrophil recruitment, degranulation and tissue damage and even asthma during chronic infection.

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HDL regulates innate and adaptive immune responses, with implications for atherosclerosis and other inflammatory diseases. Cholesterol efflux from the plasma membrane is the main mechanism. HDL proteins can also have direct effects on immune cells.

Endocannabinoids are key bioactive components of the endocannabinoid system, and the profound influence of endocannabinoids on the modulation of the immune system is being increasingly appreciated. Endocannabinoids seem to exert both anti-inflammatory and pro-inflammatory effects in specific contexts; thus, knowledge on endocannabinoid–immune cell crosstalk will pave the way to therapeutic implications of modulators of this pathway in autoimmune and chronic inflammatory disorders.

SLE-MPs contained decrease levels of miR-146a compare with HC. The miR-126 content in aSLE-MPs was increase. The treatment of U937 cells with MPs from HCs and patients increased miR-126 levels and decreased miR-146a content.

We have used bovine MHC II tetramers and PBMC from cattle vaccinated against foot-and-mouth disease (FMD) to identify novel CD4+ T-cell epitopes in the capsid of FMD virus (FMDV) and to confirm the presence of long-lasting FMDV-specific CD4+ T cells. Ex vivo analyses revealed the presence of CD45RO+CCR7+ central memory cells in higher frequency and epitope-expanded T-cell populations produced IFN-γ in vitro indicating a Th1 cell phenotype. This work indicates an important role in maintaining cell adaptive immunity after FMD vaccination and contributes to our understanding of vaccine efficacy.

Cytomegalovirus (CMV) is a potentially exciting vaccine vector, but pathogenicity may preclude the use of replicating viruses. Here, we show that a spread-deficient CMV vector is attenuated in the ability to induce T-cell memory formation after subcutaneous immunization. This results in pronounced loss of polyfunctional T cells, possibly linked to reduced development of TCF1-expressing T cells.

Butyrate and propionate but not acetate induced the apoptosis, degranulation and IL-13 expression of human basophils. Propionate and butyrate promoted histone acetylation of human basophils. Suppression of histone deacetylation by trichostatin A induced the apoptosis, degranulation and IL-13 expression of human basophils.

Investigation of the role of the immunoreceptor CD300a in the resolution of articular inflammation triggered by MSU crystals in mice. Absence of CD300a delayed resolution of neutrophilic inflammation and activation of CD300a induce neutrophil apoptosis via caspase 8.

TLR2 dimer-specific ligands selectively induce PKC isoforms activation. L. major impairs PKC phosphorylation and membrane translocation in macrophages. TLR2-ligand + PKC inhibitor co-treatments alter parasite load and Th subset response.

Graft-versus-host disease is a life-threatening complication of bone marrow transplantation. Post-transplant cyclophosphamide (PTCy) reduces clinical GVHD, but the mechanism is unclear. Using a humanized mouse model of GVHD, we demonstrate that PTCy not only reduces GVHD alongside reactive donor T cells in the liver, but also reduces human regulatory T cells, which are protective against disease.

Effects on immune responses from human PBMC exposure to type A or type B oligomers. Modelling of Alzheimer's disease and Parkinson's disease features.

Pristane can cause obvious damage to the blood vessels of ApoE−/− mice, the pathological morphology of the arterial tissue of the SLE mouse model is disordered, and the basement membrane is thickened. The treatment of IFN-α-NA reverses these phenotypes. The expression of IFN-α receptor in the vascular endothelium is increased, and that of SA-β-Gal-positive EPCs in vascular endothelium is enhanced.

ZIKV-immune sera efficiently opsonize CEM-NKR cell lines expressing ZIKV NS1. Sera from immune donors can induce both NK cell degranulation and lysis of ZIKV NS1 CEM-NKR cells in vitro.