Volume 218, Issue 3, December 2024

Spectral flow cytometry comprehensively identified the cellular composition and phenotype of each cell subsets in synovial fluid of active JIA. Compared with blood, the inflamed joint contained highly activated cell subtypes with altered co-receptor expression. The presence of certain molecules and subsets of immune cells identified offers new therapeutic avenues to specially target the inflamed site in JIA.

As a pivotal cytokine, IL-22 plays a crucial role in the pathogenesis of autoimmune diseases. In this comprehensive review, we initially provide an overview of the diverse biological functions exerted by IL-22 across various cell types and subsequently delve into its intricate involvement in numerous autoimmune disorders. Lastly, we address the current challenges and potential future directions pertaining to IL-22-related therapeutics.

Neutrophil extracellular traps (NETs) released by neutrophils are web-like DNA structures adhered to granulin proteins with bactericidal activity and can be an important mechanism for preventing pathogen dissemination or eliminating microorganisms. However, they also play important roles in diseases of other systems, such as the central nervous system. We tracked the latest advances and performed a review based on published original and review articles related to NETs and neurological diseases. Generally, neutrophils barely penetrate the blood–brain barrier into the brain parenchyma, but when pathological changes such as infection, trauma, or neurodegeneration occur, neutrophils rapidly infiltrate the central nervous system to exert their defensive effects. However, neutrophils may adversely affect the host when they uncontrollably release NETs upon persistent neuroinflammation. This review focused on recent advances in understanding the mechanisms and effects of NETs release in neurological diseases, and we also discuss the role of molecules that regulate NETs release in anticipation of clinical applications in neurological diseases.

This study demonstrates the presence of six non-criteria antiphospholipid antibodies, anti-cardiolipin antibodies IgA, aβ2-GPI IgA, aβ2-GPI Domain 1, aPS/PT, aVim/CL, aCarb-β2-GPI antibodies in a large cohort of ‘seronegative’ antiphospholipid syndrome (SN-APS) patients. They revealed potential usefulness in the identification of a significant proportion of SN-APS. Patients tested positive showed a higher prevalence of recurrent thrombosis, foetal deaths, or spontaneous abortions, suggesting that this test may be considered a suitable approach in the evaluation of SN-APS patients.

The purpose of this study was to evaluate two newly developed bioluminescent immunoassays using Lumit® (Promega) technology as a diagnostic test for AOID with AIGA. Both bioluminescent inhibition immunoassays were able to clearly discriminate between AOID with AIGA patients and healthy controls. The mean inhibition percentage between patient groups correlated with disease activity. Both assays appeared to be more sensitive when compared to the existing inhibition ELISA.

Acquired aplastic anemia (AA) often results from immune destruction of hematopoietic stem and progenitor cells. However, only 60%–70% of patients with AA respond to immunosuppressive therapy (IST). There is a lack of strong predictive markers for response to IST which can help therapy. Our study sought to pinpoint unique immune markers in AA patients and validate established predictors for response to IST.

Circulating interferon lambda cytokines (IFNL1, IFNL2, and IFNL3) were all detected in response to SARS-CoV2 infection. However, patient plasma showed reduced levels of IFNL1 and/or IFNL2 with increased disease severity.

An IFN-I signature does not distinguish GCA and PMR patients from controls. Also, IFN-I-induced serum markers are not upregulated in GCA and PMR patients. Easily measurable IFN-I-induced serum markers will therefore probably not aid in diagnosis and additional treatment options in newly diagnosed GCA and PMR patients.

In our study, we observed that the pan-PADs inhibitor, Cl-amidine significantly reduced the cardiovascular lesions (aortitis, coronary arteritis, and abdominal aorta dilation/aneurysms) in the Lactobacillus casei cell wall extract (LCWE)-induced mouse model of Kawasaki disease vasculitis. While Pad4 KO mice were not protected, treatment of these mice with a PAD2 inhibitor (AFM30a) significantly reduced cardiovascular lesions, while the PAD2 inhibitor alone in wild-type mice had no protective effect. These observations suggest a redundant role of PAD2 and PAD4 in this experimental model of Kawasaki disease vasculitis.

Psoriasis is a chronic, inflammatory skin disease characterized by a dysregulated immune response and systemic inflammation. Up to one-third of patients with psoriasis have psoriatic arthritis. We here explored the impact of long-term infliximab treatment on the composition and activity status of circulating immune cells involved in chronic skin and joint inflammation.