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Cyclic citrullinated peptide

Cyclic citrullinated peptide (CCP) is a biomarker commonly used to detect and monitor rheumatoid arthritis, an autoimmune disorder characterized by chronic inflammation of the joints.
CCP antibodies are present in the majority of rheumatoid arthritis patients and can be detected even before the onset of clinical symptoms.
The cyclic nature of the peptide enhances its binding to rheumatoid arthritis-specific autoantibodies, making it a sensitive and specific tool for disease diagnosis and prognosis.
Reserachers can leverage PubCompare.ai to streamline their CCP research, optimizing protocols and enhancing reproducibility through AI-driven comparisons of published literature, preprints, and patents.

Most cited protocols related to «Cyclic citrullinated peptide»

Nested Case-Control Study of Pre-Rheumatoid Arthritis Autoimmunity

Cited 9 times

A nested case–control study was performed within the Northern Sweden Health and Disease Study (NSHDS) and the Maternity cohort of Northern Sweden. All adult individuals of the county of Västerbotten were invited to participate; consequently, the cohorts are population-based and no individual was excluded. The NDHDS cohort consists of three subcohorts, which, together with conditions for recruitment into the cohorts and the collection and storage of blood samples, have previously been described in detail [3 ]. The registry of patients who fulfilled the American College of Rheumatology classification criteria for RA [1 (link)] and who attended the Department of Rheumatology, University Hospital, Umeå (the only medical centre for rheumatology in the county of Västerbotten), and with a known date of onset of symptoms or signs of joint disease, was coanalysed with the registers of the cohorts from the Blood Bank for Västerbotten located in Umeå. At the time of the study, the median duration of disease since the diagnosis of RA was 3.0 years (interquartile range [IQR] 1.8–5.8 years). Eighty-six individuals were identified from the cohorts as having donated blood samples before the onset of symptoms or signs of joint disease. Samples from three individuals were not available. Of the remaining 83 individuals (referred to here as 'prepatients'), blood samples for DNA analysis were available only from the NSHDS cohort, resulting in 59 prepatients (45 women and 14 men); the Maternity cohort did not include collection of samples for DNA analysis. Power calculations showed that two controls per patient would be sufficient, based on pretest probability of our previous results of HLA-DR4 frequencies in patients and controls from this area [5 ]. Therefore, we selected for genetic analysis two controls (out of the four who were previously analysed for antibody titres [3 ]) for every prepatient. The controls were randomly selected from the same subcohorts as the original cases within the NSHDS cohort and matched for sex, for age at the time of blood sampling, and for area of residence (rural or urban). The mean age of the prepatients at the time of blood sampling was 53 years (range 31–67 years) and of the controls, 53 years (range 30–67 years). The median sampling time before onset of symptoms of joint disease was 2.0 years (IQR 0.9–3.9 years). The antedating time for the samples was calculated to the onset of any symptoms of RA in all prepatients. Additional samples were collected from the prepatients at their first visit to the early-arthritis clinic (n = 52), i.e. when RA was diagnosed. On average, the diagnosis of RA was established 7.1 ± 2.8 (SD) months after the first symptoms of joint disease. The mean age at the onset of disease was 56.6 years, range 34–68 years. The Ethics Committee approved this study at the University Hospital, Umeå, and the blood donors to the Blood Bank had given their written informed consent.
HLA-DRB1 genotyping was performed using polymerase chain reaction sequence-specific primers from DR low-resolution kit and DRB1*04 subtyping kit (Olerup SSP AB, Saltsjöbaden, Sweden). The SE genes were defined as DRB1*0404 and DRB1*0401. Samples for DNA analysis from one prepatient and three controls were not available, and HLA typing of one prepatient and two controls was unsuccessful. Consequently, results of HLA typing were available from 57 prepatients and 112 controls.
The anti-CCP2 (Mark2) antibodies and the RFs were determined using enzyme-linked immunoassays as previously described [3 ].

Berglin E., Padyukov L., Sundin U., Hallmans G., Stenlund H., van Venrooij W.J., Klareskog L, & Dahlqvist S.R. (2004). A combination of autoantibodies to cyclic citrullinated peptide (CCP) and HLA-DRB1 locus antigens is strongly associated with future onset of rheumatoid arthritis. Arthritis Research & Therapy, 6(4), R303-R308.

Publication 2004

Autoantibody Testing for Rheumatoid Arthritis

Cited 8 times

Testing for RA-related autoantibodies is performed at the University of Colorado Division of Rheumatology Clinical Research Laboratory (Clinical Laboratory Improvements Amendments [CLIA]-certified). Testing is performed for the RF isotypes IgM, IgG, and IgA by ELISA assays using QUANTA Lite^™ kits, and results are reported in units per milliliter (U/mL). RF is also measured by nephelometry (RF-Neph) according to manufacturer’s specifications (Dade Behring, Newark, Delaware, USA). A positive RF (ELISA isotypes or by nephelometry) is defined as the level present in 5% or less of healthy controls according to ACR RA criteria (32 (link)). Cut-offs for RF positivity have been established using 490 randomly selected healthy blood donors from the Denver area.
Antibodies against citrullinated peptides are tested by ELISA using the anti-cyclic citrullinated peptide (anti-CCP)-2 kit (Diastat, Axis-Shield, Dundee, Scotland, UK). Per the manufacturer’s specifications, a positive test is defined as ≥5 U/mL. For all autoantibody assays, 5% of antibody negative samples as well as all positive results are re-tested and confirmed by blinded duplicate analysis.

Kolfenbach J.R., Deane K.D., Derber L.A., O’Donnell C., Weisman M.H., Buckner J.H., Gersuk V.H., Wei S., Mikuls T.R., O’Dell J., Gregersen P.K., Keating R.M., Norris J.M, & Holers V.M. (2009). A Prospective Approach to Investigating the Natural History of Pre-Clinical Rheumatoid Arthritis (RA) Using First-Degree Relatives of Probands with RA. Arthritis and rheumatism, 61(12), 1735-1742.

Publication 2009

3,3'-diallyldiethylstilbestrol Antibodies Autoantibodies Biological Assay Clinical Laboratory Services cyclic citrullinated peptide Donor, Blood Enzyme-Linked Immunosorbent Assay Epistropheus Immunoglobulin Isotypes Immunoglobulins Nephelometry Peptides

Rheumatoid Arthritis Inclusion Criteria

Cited 8 times

At enrollment, entry criteria included disease duration < 3 years from the time of diagnosis; age over 18 years; RA diagnosis by the 1987 ACR criteria (20 (link)); active disease (at least 4 swollen and 4 tender joints, using the 28-joint count); positive for rheumatoid factor (RF) or cyclic citrullinated peptide (CCP) antibodies, or if seronegative, have at least 2 erosions by radiographs of hands/wrists/feet; if taking corticosteroids, receiving stable doses at least 2 weeks prior to screening (≤ 10 mg/day of prednisone); and if taking non-steroidal anti-inflammatory drugs, receiving stable doses for at least 1 week. Exclusion criteria were contraindications to study medications; prior use of biologic therapy of any type, at any dosage; corticosteroid injections during the 4 weeks prior; and diagnosis of serious infection, including positive skin test for TB. Prior use of leflunomide, HCQ, and SSZ was allowable for no more than 2 months. Also permitted was a total dose of ≤ 40 mg of MTX.

Moreland L.W., O’Dell J.R., Paulus H.E., Curtis J.R., Bathon J.M., Clair E.W., Bridges SL J.r., Zhang J., McVie T., Howard G., van der Heijde D, & Cofield S.S. (2012). A Randomized Comparative Effectiveness Study of Oral Triple Therapy versus Etanercept plus Methotrexate in Early, Aggressive Rheumatoid Arthritis. Arthritis and rheumatism, 64(9), 2824-2835.

Publication 2012

Adrenal Cortex Hormones Anti-Cyclic Citrullinated Protein Antibodies Anti-Inflammatory Agents, Non-Steroidal Diagnosis Foot Infection Joints Leflunomide Pharmaceutical Preparations Prednisone Rheumatoid Factor Test, Skin Therapies, Biological Wrist X-Rays, Diagnostic

Genetic Factors in Early Rheumatoid Arthritis

Cited 8 times

Patients from the four northern-most counties of Sweden with early RA (duration of symptoms < 12 months) were consecutively included in the study and followed for 2 years. A total of 563 individuals fulfilling at least four of the seven American College of Rheumatology criteria for RA [18 (link)] were identified. The patients were assessed clinically at baseline and after 6, 12, 18 and 24 months using the 28-joint count for tender and swollen joints and a global visual analogue scale, and the erythrocyte sedimentation rate was measured. The Disease Activity Score (DAS28) was calculated [19 (link)]. Of the patients identified, 505 (342 females, 163 males) were willing to participate and donated DNA for this study. During the study period, 98.0% (n = 448/457) of the patients were treated for at least 6 months with disease-modifying antirheumatic drugs and 53.0% (n = 244/460) of the patients were receiving prednisolone for at least 6 months. All patients were asked by questionnaire about their smoking habits, and were defined as smoker, nonsmoker ever or previous smoker. Demographic and clinical data of the patients at baseline are presented in Table 1.
From among the 505 patients with early RA, a subcohort of 85 individuals was identified as being donors to the Medical Biobank of northern Sweden before disease onset. The median time predating disease onset was 2.7 years (interquartile range = 1.1–6.0 years). Serological analyses before and after disease onset were undertaken for these individuals. The Medical Biobank is population based, and conditions for recruitment into the cohorts and for the collection and storage of blood samples have previously been described in detail [5 (link)].
A total of 970 controls from the Medical Biobank of northern Sweden were randomly selected and matched for sex and age within a range of 5 years. The mean age of the controls was 58.2 years (range 25–79 years), and the distribution of males and females was 26.3% and 73.7%, respectively. The Regional Ethics Committee at the University Hospital at Umeå approved this study and all participants gave their written informed consent.
The DNA from patients and controls (n = 505 and n = 970, respectively) was extracted from ethylenediamine tetraacetic acid-treated whole blood using a standard salting-out method. The 5' nuclease assay was used to determine the PTPN22 1858 C/T polymorphism (single nucleotide number rs2476601) as previously described [7 (link)]. The PCRs were performed according to the manufacturers' instructions, and detection of the different genotypes was made using an ABI PRISM^®7900 HT Sequence Detector System (Applied Biosystems, Foster City, CA, USA). Data were processed using the SDS 2.1 software (Applied Biosystems). The different genotypes were verified by comparison with control samples of known genotype. Genotyping was successful for 504 of the patients.
HLA-DRB1 genotyping was performed using PCR sequence-specific primers from the DR low-resolution kit and DRB1*04 subtyping kits (Olerup SSP AB, Saltsjöbaden, Sweden) according to the previously described method [20 (link)]. The HLA-SE genes were defined as DRB1*0404 and DRB1*0401. Results of HLA-DRB1 genotyping were available for 500 patients and 170 randomly selected controls (mean age 53.0 ± 8.9 years, 74.7% females and 25.3% males).
Anti-CCP2 antibodies (n = 468 patients) were determined using the Diastat kit from Axis-Shield Diagnostics (Dundee, UK) (cutoff value = 5 units/ml). Rheumatoid factor of the IgM isotype was determined using the agglutination test with sentized sheep erythrocytes as originally described according to Waaler-Rose (n = 366).
The chi-square test was used for testing categorical data between groups. Student's t-test for independent samples was used to analyse continuous data. Binary logistic regression models were used to estimate predictive values of the 1858T variant of PTPN22, HLA-SE alleles, anti-CCP antibodies and smoking. Odds ratios (ORs) were calculated with 95% confidence intervals (CIs). All P values refer to a two-sided test, and P ≤ 0.05 was considered statistically significant. To correct for multiple comparisons, a corrected P value (P_c) is also presented. The calculations were performed using the SPSS package (SPSS for Windows 14.0; SPSS Inc., Chicago, IL, USA). The area under the curve using DAS28 values for 24 months was calculated. Any missing values were assumed to be at random; consequently, the last value forward was used for missing DAS28 values at specific time points.

Kokkonen H., Johansson M., Innala L., Jidell E, & Rantapää-Dahlqvist S. (2007). The PTPN22 1858C/T polymorphism is associated with anti-cyclic citrullinated peptide antibody-positive early rheumatoid arthritis in northern Sweden. Arthritis Research & Therapy, 9(3), R56.

Publication 2007

Biological Agents in RA Patients

Cited 8 times

UK-wide multicentre collaborations were established to recruit patients treated with anti-TNF drugs for RA. Eligible patients from each centre were subsequently identified from the British Society of Rheumatology’s (BSR) Biologics Register (BR).18 (link) This register compiles extensive clinical information on patients starting treatment with a biological agent and follows them prospectively, on a 6-monthly basis for 5 years, in order to monitor and determine the incidence of potential short and long term hazards. The following criteria were used for the selection of patients for the current study: (1) currently actively participating in the BSRBR long-term safety study, (2) doctor-confirmed diagnosis of RA, (3) currently or have been treated with one of the three anti-TNF biological agents, (4) European Caucasian descent and (5) reached 6 months of follow-up. Patients who stopped treatment temporarily during the first 6 months of therapy were excluded from selection. Similarly, patients who discontinued therapy prior to the 6-month follow-up for any reason other than inefficacy were excluded from selection.

Potter C., Hyrich K.L., Tracey A., Lunt M., Plant D., Symmons D.P., Thomson W., Worthington J., Emery P., Morgan A.W., Wilson A.G., Isaacs J, & Barton A. (2008). Association of rheumatoid factor and anti-cyclic citrullinated peptide positivity, but not carriage of shared epitope or PTPN22 susceptibility variants, with anti-tumour necrosis factor response in rheumatoid arthritis. Annals of the Rheumatic Diseases, 68(1), 69-74.

Publication 2008

Biological Factors Caucasoid Races Diagnosis Europeans Patients Pharmaceutical Preparations Physicians Safety Therapeutics

Most recents protocols related to «Cyclic citrullinated peptide»

Autoantibody Detection Using Chemiluminescence

The presence of anti-CCPs was determined by chemiluminescence using a third-generation commercial anti-CCP test (Abbott, IL, USA) and processed in an Abbott Architect Plus autoanalyzer. When the concentration was ≥20 IU/mL, samples were considered positive [18 (link),19 (link)].

Hernández-Huirache H.G., Armenta-Medina D, & Rodea-Montero E.R. (2024). Clinical, Immunological and Inflammatory Characteristics among Mexican Children with Different Subtypes of Juvenile Idiopathic Arthritis: Exploring the Correlation between Anti-Cyclic Citrullinated Peptide (anti-CCP) and Rheumatoid Factor (RF). Pediatric Reports, 16(1), 151-162.

Publication 2024

Affinity-based ACPA Purification and Profiling

For affinity-based ACPA purification, we selected the citrullinated antigen cyclic citrullinated peptide 2 (CCP2; patent number: EP2071335), a “golden standard” antigen used in clinical practice for diagnostic and prognostic purposes. The non-modified version of CCP2 (CArgP2) served to remove antibodies binding to either the column material or the peptide backbone.
ACPA fine-specificity profiles were determined using the citrullinated peptides fibrinogen α 27-43 (FLAEGGGVCitGPRVVERH), fibrinogen β 36-52 (NEEGFFSACitGHRPLDKK), cyclic citrullinated peptide 1 (CCP1; HQCHQESTCitGRSRGRCGRSGS), vimentin 59-74 (VYATCitSSAVCitLCitSSVP) and enolase 5–20 (KIHACitEIFDSCitGNPTV)^{30 (link),42 (link)}, as well as citrullinated fibrinogen and fetal calf serum (FCS). N-terminally biotinylated CCP2 and CArgP2 as well as the N-terminally biotinylated peptides to determine ACPA fine-specificity profiles were prepared (kindly provided by Dr. J. W. Drijfhout, Department of Immunology, LUMC) as described previously^{42 (link)}. Proteins were modified as described before^{43 (link)}; however, citrullination of FCS was performed at 37 °C and additionally supplemented with 2.5 M NaCl and 0.5 µM EDTA.
CCP2 and CArgP2 columns were prepared by functionalizing 1 mL HiTrap® Streptavidin HP columns (GE Healthcare/Cytiva) with 1.0–1.5 mg N-terminally biotinylated CCP2 or CArgP2 peptide at a flow rate of 0.2 mL/min. Excess of peptide was removed by washing with PBS and glycine-HCl, pH 2.5. Columns were stored in 20% ethanol until usage.

Stork E.M., van Rijswijck D.M., van Schie K.A., Hoek M., Kissel T., Scherer H.U., Huizinga T.W., Heck A.J., Toes R.E, & Bondt A. (2024). Antigen-specific Fab profiling achieves molecular-resolution analysis of human autoantibody repertoires in rheumatoid arthritis. Nature Communications, 15, 3114.

Publication 2024

Cardiovascular Risk in Rheumatoid Arthritis

Data were collected in case registration forms. Baseline data on demographic and clinical characteristics (duration of RA, RA treatment history, rheumatoid factor, and anti-cyclic citrullinated peptide antibody); carotid duplex ultrasound and PWV at baseline, Weeks 52, 104, and 156; and efficacy and laboratory parameters at baseline and Weeks 52, 104, and 156 were collected.

Yamada Z., Muraoka S., Kawazoe M., Hirose W., Kono H., Yasuda S., Sugihara T, & Nanki T. (2024). Long-term effects of abatacept on atherosclerosis and arthritis in older vs. younger patients with rheumatoid arthritis: 3-year results of a prospective, multicenter, observational study. Arthritis Research & Therapy, 26, 87.

Publication 2024

Comprehensive Rheumatoid Arthritis Assessment

Relevant data were taken from the patients, including age, sex, disease duration, and number of tender and swollen joints. Rheumatoid arthritis disease severity was assessed by the Disease Activity Score 28 (DAS28). Functional status was assessed by the Health Assessment Questionnaire (HAQ). Patient laboratory investigations, including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), rheumatoid factor (RF), and anti-cyclic citrullinated peptide antibodies (anti-CCP) were recorded.

Jahan T., Saleh A.A, & Anwar S. (2024). Association of Cytokine IL-17, IL-4, IL-6, and IL-12 Gene Polymorphisms in Rheumatoid Arthritis Patients in a Tertiary Care Hospital in Bangladesh. International Journal of Rheumatology, 2024, 3728179.

Publication 2024

Profiling Severe Rheumatoid Arthritis

Not available on PMC !

We collected basic demographic and clinical information including age, gender, smoking status, rheumatoid factor (RF) and anti-cyclic citrullinated peptide (CCP) antibody status (Supplementary Table 1). We recruited healthy volunteers for collection of peripheral blood and basic demographic information. We screened RA donors for patients for severe RA (polyarticular synovitis on exam) and designated three patients 'index patients' that were analyzed in detail to create working definitions for potentially antigenpresenting cells.

Geier C., Qudsi H., Gabr J.B., Winchester R., & Perl A. (2024). CD1c Dendritic Cells are depleted and accompanied by new HLA-DR^hiPhenotypes in Rheumatoid Arthritis Blood.

Publication 2024

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More about "Cyclic citrullinated peptide"

Cyclic citrullinated peptide (CCP) is a critical biomarker for detecting and monitoring rheumatoid arthritis (RA), an autoimmune disorder characterized by chronic joint inflammation.
CCP antibodies are present in the majority of RA patients and can be identified even before the onset of clinical symptoms.
The cyclic nature of the peptide enhances its binding to RA-specific autoantibodies, making it a highly sensitive and specific tool for disease diagnosis and prognosis.
Researchers can leverage AI-powered platforms like PubCompare.ai to streamline their CCP research, optimizing protocols and enhancing reproducibility.
PubCompare.ai allows researchers to locate the best CCP-related protocols from literature, preprints, and patents, and leverage AI-driven comparisons to improve accuracy and efficiency.
In addition to CCP, other related biomarkers and diagnostic tools are commonly used in RA management, such as the Cobas e411 analyzer, DBA/1J mice models, Phadia 250 immunoassay system, Cobas 6000 analyzer, Bio-Plex system, CardioPhase hsCRP assay, BN II System, Immage 800 analyzer, and QUAN-TA-Lyser 2 system.
These technologies and platforms can be utilized to complement CCP testing and provide a more comprehensive understanding of RA progression and treatment response.
By optimizing CCP research workflows and leveraging the latest advancements in diagnostic tools, researchers can streamline their discoveries and take their work to new heights, ultimately improving the lives of individuals affected by rheumatoid arthritis.