Characterization of RA33 (hnRNP-A2/B1)-autoreactive T cells in SLE-patients

Abstract

We discuss the presence of anti-keratin antibodies (AKA) of the IgG class in patients with defined juvenile idiopathic arthritis (JIA). An indirect immunofluorescence test and rat oesophagus substrate was used for the detection and quantification of AKA antibodies in patients´ sera. Overall 33/60 patients with JIA had sera positive for AKA (55 %, P = 0,0001) ranging from 1:10 to 1:160 dilutions. Following idiopathic arthritis of childhood classification criteria AKA occurred in 2/7 patients with systemic disease (28,6 %), in 13/30 patients with RF negative polyarthritis (43,3 %, P = 0,008) and in 15/18 RF positive polyarthritis (83,3 %, P = 0,000002). AKA were also found in a small cohort of patients with oligoarthritis (1/3) and psoriatic arthritis (2/2). AKA positivity occurred in 3/26 healthy controls at a 1:20 dilution. The presence of AKA was correlated as well as with the severity of the disease. Our study revealed that AKA was present overall in 18/29 patients (62%) with severe JIA and in 12/26 patients (46,2 %) with non-severe disease, however this did not reach statistical significance (P = 0,18). We also observed that AKA remained positive regardless of disease activity. AKA were detectable in 55,6 % patients with active JIA and in 48,6 % patients in the complete or near remission. Acknowledgement: This research was supported by a European Commission (Acronym: EUROBANK, contract no: QOL-2000-14.1), web site http://www.ncl.ac.uk and by grant of 2nd Medical Faculty, Charles University in Prague, VZ no. 111300003. P2The significance of antibodies to cyclic citrullinated peptide, antikeratin antibodies, antiperinuclear factor, rheumatoid factor isotypes and HLA shared epitope in prediction of erosive disease in early rheumatoid arthritis patients J Vencovsky, L Sedova, S Machacek, J Gatterova, V Pesakova, J Kafkova and O Krystufkova Institute of Rheumatology, Prague, Czech RepublicObjectives: To evaluate a predictive value of autoantibody examinations in development of erosive disease in early rheumatoid arthritis (RA). Patients and methods: One hundred and fourteen patients with disease duration less than 2 years after the onset of symptoms were investigated. Only patients who fulfilled the diagnostic criteria for RA either at the beginning of the disease or during the follow-up period were included. The antibodies to cyclic citrullinated peptide (anti-CCP) (Immunoscan RA, Euro-diagnostica, The Netherlands), IgM, IgA and IgG rheumatoid factors (RF) were measured by ELISA, antikeratin antibodies (AKA) and antiperinuclear factor (APF) were detected by indirect immunofluorescence, and the presence of HLA shared epitope (HLA SE) was detected by PCR with sequence specific primers. Patients were divided into two groups, either with erosive or non-erosive changes present on the hand or/and feet radiographs at the end of 24 months follow-up. Results: Seventy-six (66.7%) patients developed bony erosion, whereas 38 (33.3%) remained without destructive changes. The initial anti-CCP, AKA, APF, IgM RF, IgA RF, IgG RF ...

Human T cell clones specific for heterogeneous nuclear ribonucleoprotein A2 autoantigen from connective tissue disease patients assist in autoantibody production

“…Recently, we and another group reported preliminary findings describing the identification of human T cells reactive with hnRNP antigen (4,5). Fritsch and colleagues subsequently identified and studied hnRNPreactive T cells from patients with RA and reported that these T cells exhibited a Th1-like phenotype and were largely restricted in antigen recognition by HLA-DR molecules (6).…”

Undervalued and novel roles of heterogeneous nuclear ribonucleoproteins in autoimmune diseases: Resurgence as potential biomarkers and targets

“…Besides, autoreactive T cell clones against RA33 isolated from RA patients demonstrated an inclination toward Th1 phenotype with a strong production of IFN‐γ (Fritsch et al, 2002). Likewise, the PBMCs from SLE patients exhibited pronounced proliferative responses to hnRNP A2, and the T cell clones specific for hnRNP A2 encompassed high frequency of CD8 + CD28 − subsets which predominantly secreted interleukin (IL)‐10 (Fritsch‐Stork et al, 2006). In this regard, seeking ways that directly or indirectly hold down the aberrant expressions of hnRNPs or hnRNPs‐evoked immune responses may lead to therapeutic alternatives for specific autoimmune disorders, exemplified by the suppression of upregulated hnRNP A2/B1 in HDMECs induced via BD‐associated stimulants when treated with cilostazol (An et al, 2017).…”