The broad spectrum of interactions between autoimmune diseases and the SARS-CoV-2 vaccination is not fully understood. This study aims to evaluate the prevalence of anti-nuclear antibodies (ANA), anti-ENA, anticardiolipin antibodies (ACL), and anti-beta-2 glycoprotein I antibodies (anti-β2GPI) before and after the SARS-CoV-2 mRNA vaccination in a real-life setting in healthcare professionals. The identification of risk factors associated with vaccine immunogenicity was evaluated. The study group consisted of employees of two hospitals (354 individuals). Samples for antibody assays were collected before vaccination and at 7–9 months after complete immunisation. There was no significant increase in the prevalence of ANA, ACL or anti-β2GPI antibodies, or autoimmune diseases in subjects who were vaccinated 7–9 months after complete immunisation. In terms of detected anti-ENA, the anti-DFS70 antibodies were found in 6 times more subjects than before vaccination at the second blood draw (in 18 and 3 subjects, respectively) (p = 0.001). There were no significant relationships between a SARS-CoV-2 infection history, humoral response, cellular response, subject category, smoking, sex, body weight, ANA, anti-ENA, ACL, or anti-β2GPI. This study revealed a possible association between the severity of vaccine adverse events (VAEs) and ANA titre. Individuals with more severe VAEs (>10 points) after the second dose of the vaccine had significantly higher ANA titre after complete immunization. When analysing the significance of time between the ANA, anti-ENA, ACL, and anti- β2GPI assays and complete immunisation antibody values, no qualitative result was statistically significant. There was correlation between the time since complete immunization and ANA after.

Vaccination is the best way to limit the extent of the COVID pandemic. Knowledge of the duration of the immune response will allow the planning of a vaccination protocol. This study aims to validate the complete (humoral and cellular) immune responses over time in large population groups following the full vaccination of healthcare professionals in real-life conditions and to assess the relationship between antibody levels and T-cell activity in relation to the characteristics of the study group. The samples for the study were obtained from volunteers (staff of two hospitals) on three occasions: before vaccination, T0, then 4–9 weeks after full vaccination (two doses BNT162b2), T1, and 7–9 months after vaccination, T2. The humoral response was investigated by the titre of anti-SARS-CoV-2 IgG antibodies to S1 protein. Assays were performed three times at intervals. The cellular response was assessed in a subgroup of 189 subjects by QuanT-Cell SARS-CoV-2 (IGRA). The assay was performed once. A group of 344 subjects fully vaccinated with the BNT162b2 vaccine were included in the study. The humoral response was observed in 100% of subjects at both 4–7 weeks and 7–9 months, but antibody titres fell by almost 90% in this interval. The cellular response was observed in 94% (177/189) of subjects 7–9 months after the second dose of vaccine. In subjects with a negative cellular response, eight out of 12 smoked. A factor associated with greater immunogenicity of vaccination was past SARS-CoV-2 infection. The administration of full BNT162b2 vaccination (two doses) induces humoral and cellular responses detectable even more than six months after vaccination. Smoking may be a factor associated with impaired cellular response to vaccination.

Introduction: The purpose of the study was to investigate whether single-nucleotide polymorphisms (SNPs) IL-6 − 174 G/C and IL-6R Asp358Ala are associated with susceptibility to psoriatic arthritis (PsA) or affect response to treatment with methotrexate (MTX). Patients and Methods: Seventy-four patients diagnosed with PsA and qualified for MTX treatment were enrolled to the study. The control group consisted of 120 healthy individuals. Polymorphisms IL-6 − 174 G/C and IL-6R Asp358Ala were genotyped using a polymerase chain reaction (PCR) amplification employing LightSNiP assays. Results: A significant association between the IL-6 − 174 CC genotype and an improved clinical outcome of MTX therapy was observed. A good response was more frequently observed among PsA patients bearing the IL-6 − 174 CC genotype than patients with the GC or GG genotypes (P = 0.007). On the other hand, patients carrying the IL-6 − 174 GC genotype less frequently responded to MTX treatment as compared to patients with other genotypes (P = 0.006). With respect to the IL-6R Asp358Ala SNP, there were no significant differences in genotype and allelic frequencies in relation to clinical outcome of MTX treatment. No association was found between the IL-6 − 174 G/C or IL-6R Asp358Ala SNPs and PsA susceptibility. Conclusion: Results from this study provide evidence that the IL-6 − 174 G/C polymorphism might influence efficacy of MTX treatment.

Psoriatic arthritis (PsA) and rheumatoid arthritis (RA) are connective tissue autoimmune diseases. The present study aimed to check whether serum clusterin (CLU) concentration and its glycosylation pattern may be markers differentiating these diseases—blood sera of patients with PsA (n = 37), RA (n = 34), and healthy subjects (control, n = 21) were examined. CLU concentration was measured using the ELISA test. Glycosylation was analyzed using lectin-ELISA with sialo-specific lectins from Maackia amurensis (MAA) and Sambucus nigra (SNA) recognizing sialic acid (SA) α2,3- and α2,6-linked, respectively, and fucose-specific lectins from Lotus tetragonolobus (LTA), Ulex europaeus (UEA), and Lens culinaris (LCA) specific to fucose α1,3-linked, α1,2-linked, and core fucose, respectively. Significantly higher CLU concentrations were observed in the PsA than in the RA patients. The expression of α2,6-linked SA was significantly higher in the PsA and RA patients than in the control. The expression of SNA-reactive SA was visibly higher in the PsA compared to the RA and control group but insignificant. Negative significant correlations between CLU concentrations and its glycans reactivity with LTA and UEA were also observed. Significantly higher serum CLU concentration, accompanied by a high expression of SNA-reactive SA and a reduced degree of Lewis^x and Lewis^y antennary fucosylation, may constitute a promising panel of parameters differentiating PsA from RA.

Background The first reports on the differences in glycosylation, which may negatively affect the antibody function, came from the studies on rheumatoid arthritis (RA), and specifically, the occurrence of glycoform G0 (no galactose) [1]. The increase of agalactosylated IgG in patients with other diseases (juvenile arthritis, Crohn’s disease) [2] was also found. It is known, that the percentage of IgG agalactosyled N-glycans in RA increases with the disease progress, and returns to normal in the remission phase; both features were confirmed in the previous studies conducted in our laboratory [3]. Objectives The aim of this study was to evaluate agalactosylation factor (AF) in patients with PsA during biological treatment at Rheumatology Clinic, Medical University in Wroclaw. Patients were treated with adalimumab in combination with MTX, NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) or cyclosporine under permission of the Commission of Bioethics (Medical University, Wroclaw, Poland). The patients between 26-61 years old (mean 48) were diagnosed by the criteria recommended by CASPAR group. Methods Immunoglobulin G was isolated from the serum samples using a column of Sephadex G-25 and DE52 anion exchange resin. The galactosylation of serum IgG was determined using an ELISA-plate test, with two lectins Ricinus communis (RCA-I) and Griffonia simplicifolia (GSL-II), separately. The IgG control was prepared from the pooled serum samples of 5 healthy persons. Triplet wells on a microplate were used for one sample. The ELISA- plate test was performed as previously described [3]. Results The relative binding of GSL –II and RCA –I was expressed as the absorbance given by tested sample, divided by the absorbance of the control sample; the ratio of relative GSL –II/RCA –I binding was termed as agalactosylation factor (AF) [3]. We determined AF for IgG samples and a control sample. The AF of control was set to 1.0; we have previously [3] confirmed the AFs of IgG of healthy individuals are close to 1. The AF value for 5 patients decreased during therapy and this correlated with a concomitant decrease of initially elevated clinical parameters and with general improvement of patients’ health. The AF value of Bor was comparatively less elevated at the beginning of treatment and insensibly increased. Conclusions The studies have shown higher AF in PsA patients compared to control (healthy people). During therapy with adalimumab decrease of AF was observed, which meant increase of galactosylation of IgG. We plan to perform tests on a larger group of patients. Parekh, R.B. et al., Association of rheumatoid arthritis and primary osteoarthritis with changes in the glycosylation pattern of total serum IgG, Nature, 316; 452-457; 1985; Rademacher, T.W., Williams, P., Dwek, R.A., Agalactosyl glycoforms of IgG autobodies are pathogenic, Proc. Natl. Acad. Sci. USA, 91, 6123-6127, 1994; Pasek, M. et al., Galactosylation of IgG from rheumatoid arthritis (RA) patients – changes during therapy, Glycoconj. J., 23, 463-471, 2006; Disclosure of Interest None Declared

Systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) are autoimmune diseases that frequently coexist, complicating clinical management due to the compounded risks of systemic inflammation and thromboembolism. We present a case of a 52-year-old female with SLE and APS, initially diagnosed after a pulmonary embolism in 2015. Her medical history includes recurrent anemia, hyperlipidemia, hypertension, and two myocardial infarctions treated with angioplasty and stenting. Despite treatment with hydroxychloroquine, methylprednisolone, methotrexate and apixaban (later switched to warfarin), the patient experienced severe disease flare-ups and cardiovascular complications, prompting consideration for biologic therapy with anifrolumab. This case study illustrates the difficulties associated with the management of concurrent SLE and APS. It is clear that early diagnosis, vigilant monitoring, and aggressive management of both autoimmune and cardiovascular risks are essential to improve patient outcomes.