Volume 211, Issue 3, March 2023

The N-terminal domain of Three Prime Repair Exonuclease 1 (TREX1) is catalytically active and can degrade dsDNA or ssDNA in the cytosol, whereas the C-terminal domain is primarily involved in protein localization. TREX1 deficiency induces cytosolic DNA accumulation as well as activation of the cGAS-STING-IFN signaling pathway, which results in tissue inflammation and autoimmune diseases. Furthermore, TREX1 expression in cancer immunity can be adaptively regulated to promote tumor proliferation, making it a promising therapeutic target.

The concept of how autoimmunity occurs in rheumatoid arthritis is changing. Besides autoantigen recognition, the responsiveness of T cells and macrophages is determined by their bioenergetics and their biosynthetic commitment. Mitochondria are emerging as critical drivers of autoimmunity by controlling production of energy and metabolites and by regulating the communication of subcellular organelles.

The impact of HLA-DQ2/DQ8, the main genetic risk factor for accelerating progression from 1 to multiple autoantibodies, largely depended on CTLA4 status in the Belgian cohort.

We compared a TRPV2 agonist with etanercept. Both achieved similar effects in suppressing arthritis and reducing joint damage. The combination of both agents was superior than the monotherapies.

Proposed mechanisms of neutrophil extracellular trap (NET) inhibition by CQ and HCQ. Chloroquine (CQ) and hydroxychloroquine (HCQ) inhibit NET formation through direct inhibition of PAD4, which is responsible for unwinding and release of DNA from neutrophils. When considered with regard to the established function of CQ/HCQ in autophagy inhibition and of the role of autophagy in NETs, we suggest two independent mechanisms for NET inhibition by these drugs, through blockade of autophagy or inhibition of PAD4.

Macrophage polarization is a critical component of tissue homeostasis, disease processes, and resolution. This report describes features of macrophage polarization using a nonhuman primate model of experimental periodontitis. The results show clear features of macrophage phenotype in health, disease, and resolution and identify alterations with age.

PanAd3 vaccination of healthy adults induces type-1 interferon and humoral immune responses.

Total spike-specific IgG antibody responses after two doses of ChAdOx1 nCov-19 (AZD1222) persist well for 1 year. Modelling suggesting titres are well maintained for at least 2 years. Therefore, two doses of ChAdOx1 nCov-19 will likely have a positive impact against serious disease and hospitalization.

Epicutaneous application of mannan mixed with incomplete Freund’s adjuvant induced clinical symptoms of plaque psoriasis in inbred mice. Although certain similarities and differences exist in the involvement of neutrophils, macrophages, dendritic cells, Vγ4 T cells, and pro-inflammatory cytokines between mannan- and imiquimod-induced psoriasis-like inflammation, former model was more severe with a better relapsing disease feature and treatment response. In addition, mannan-induced psoriasis is relatively easy to induce, economical and less harmful to mice with an increased possibility to develop a chronic psoriasis model in mice with repeated exposures.