<b>Objective:</b> To characterize the rate of healthcare resource utilization (HCRU) between anti-cyclic citrullinated peptide (CCP; a surrogate for anti-citrullinated protein antibodies [ACPAs]) positive (+) patients with rheumatoid arthritis (RA), either with or without erosions, who initiated biologic disease-modifying antirheumatic drug (bDMARD) treatment.
Recent phenotypic studies describe the possible implication of a novel subset of peripheral T helper cells (Tph) important for T-B cell cross talk and plasma cell differentiation in the RA joint of ACPA+ (autoantibodies against citrullinated proteins) RA patients.
High SF granulocyte-derived MP were observed in patients with established RA (n = 24), ACPA-positive RA (n = 32) compared to their negative counterparts (p = 0.03; p = 0.02, respectively).
B cell-rich patients showed higher levels of disease activity and sero-positivity for RF and ACPA in early RA but not in establishedRA, while significantly higher histologic synovitis scores in B cell-rich patients were demonstrated in both cohorts.
In this study, we profiled MHC-specific methylated CpGs in autoantibody-positive RA patients and matched unaffected autoantibody-negative first-degree relatives (ACPA-/FDR) from an Indigenous North American (INA) population that is known to have prevalent RA.
Anti-citrullinated protein antibodies (ACPA)s are a hallmark of rheumatoid arthritis (RA) and are essential for serological diagnosis of RA.ACPAs are not specific for a single citrullinated target; in fact, several citrullinated ACPA target proteins have been described.
The aims of study were to evaluate: the prevalence of ILD involvement in RA over high-resolution computed tomography (HRCT); the relationships between pulmonary function tests (PFTs), patient-centered measurements, and ILD; and the potential risk factors contributing to RA-ILD patients.Data regarding the clinical characteristics (age, sex, age at onset of RA), laboratory findings (rheumatoid factor [RF] and anti-citrullinated protein antibodies [ACPA]), respiratory functional assessment (forced vital capacity [FVC] and carbon monoxide diffusion capacity [DLCO]), patient-centred measures of dyspnea (PCMD), Health Assessment Questionnaire-Disability Index (HAQ-DI), and HRCT have collected retrospectively.
However, just as innate and adaptive immunity are closely functionally integrated, some ACPA+ RA cases have superimposed "autoinflammatory" features including abrupt onset attacks, severe attacks, self-limiting attacks, relevant autoinflammatory mutations or SNPs and therapeutic responses to autoinflammatory pathway therapies including colchicine and IL-1 pathway blockade.
The vitamin D metabolite 1,25(OH)<sub>2</sub> D was inversely associated with disease activity and positively associated with ACPA in treatment naïve and inflammatory active early RA.
Moreover, PR3 is a serine protease whose membrane expression can potentiate inflammatory diseases such as ANCA-associated vasculitis and rheumatoid arthritis.
IL-7 remains a potential biomarker for ACPA-negative RA although further validation with larger numbers of ACPA-negative patients is still needed notably to translate these results into clinical applicability.
The presence of abnormal B cell and autoantibodies produced by most RA patients, primarily ACPA and RF, indicate that the function of B cell was involved in the development of RA disease.
In anti-citrullinated protein antibody positive rheumatoid arthritis (ACPA-positive RA), a particular subset of <i>HLA-DRB1</i> alleles, called shared epitope (SE) alleles, is a highly influential genetic risk factor.
Anti-CD26 levels were increased approximately two-fold for each isotype in RA, were not related to the sCD26 clearance, showed several correlations with disease activity parameters, were significantly higher in smokers and they were not ACPA.
Target antibodies were isolated from RA patient plasma (polyclonal ACPA- and non-ACPA-IgG) or recombinantly produced to obtain monoclonal IgG with well-defined Fc galactose content.
In this study, the relationships between RANKL and ACPA, anti-carbamylated protein antibodies (anti-CarP), cytokines and chemokines were analysed in individuals before the onset of RA symptoms, and their associations with radiological findings at disease onset were assessed.
A total of 924 ACPA-positive RA patients with joint damage in hands and/or feet, and 1524 healthy controls were genotyped in 582 591 single-nucleotide polymorphisms (SNPs) in the discovery phase.