You will be shown a scientific claim, and the abstract of a biomedical research paper. Each sentence from the abstract will be on a separate line. Your task is to return a JSON object with two fields:

- "verdict": The fact-checking verdict. If the information in the abstract supports the claim, write "SUPPORT". If the abstract contradicts the claim, write "CONTRADICT". If the abstract does not provide enough information to arrive at a verdict, write "NEI" (for "not enough information").
- "evidence": An array of sentences providing evidence for the verdict. Please copy all relevant sentences verbatim from the abstract. If the verdict was "NEI", then return an empty array.

For instance, if the model were given the claim "smoking causes cancer", the output might be
{
  "verdict": "SUPPORT",
  "evidence": ["The results of our meta-analysis provide overwhelming support that cigarette smoking is a risk cause for lung cancer."]
}

Your response should not include any text other than the json.

Claim: Citrullinated proteins externalized in neutrophil extracellular traps act indirectly to perpetuate the inflammatory cycle via induction of autoantibodies.

Abstract:
The early events leading to the development of rheumatoid arthritis (RA) remain unclear, but formation of autoantibodies to citrullinated protein antigens (ACPAs) is considered a key pathogenic event.
Neutrophils isolated from patients with various autoimmune diseases display enhanced neutrophil extracellular trap (NET) formation, a phenomenon that exposes autoantigens in the context of immunostimulatory molecules.
We investigated whether aberrant NETosis occurs in RA, determined its triggers, and examined its deleterious inflammatory consequences.
Enhanced NETosis was observed in circulating and RA synovial fluid neutrophils compared to neutrophils from healthy controls and from patients with osteoarthritis (OA).
Further, netting neutrophils infiltrated RA synovial tissue, rheumatoid nodules, and skin.
NETosis correlated with ACPA presence and levels and with systemic inflammatory markers.
RA sera and immunoglobulin fractions from RA patients with high levels of ACPA and/or rheumatoid factor significantly enhanced NETosis, and the NETs induced by these autoantibodies displayed distinct protein content.
Indeed, during NETosis, neutrophils externalized the citrullinated autoantigens implicated in RA pathogenesis, and anti-citrullinated vimentin antibodies potently induced NET formation.
Moreover, the inflammatory cytokines interleukin-17A (IL-17A) and tumor necrosis factor-α (TNF-α) induced NETosis in RA neutrophils.
In turn, NETs significantly augmented inflammatory responses in RA and OA synovial fibroblasts, including induction of IL-6, IL-8, chemokines, and adhesion molecules.
These observations implicate accelerated NETosis in RA pathogenesis, through externalization of citrullinated autoantigens and immunostimulatory molecules that may promote aberrant adaptive and innate immune responses in the joint and in the periphery, and perpetuate pathogenic mechanisms in this disease.
{"verdict": "SUPPORT", "evidence": ["Indeed, during NETosis, neutrophils externalized the citrullinated autoantigens implicated in RA pathogenesis, and anti-citrullinated vimentin antibodies potently induced NET formation.", "Moreover, the inflammatory cytokines interleukin-17A (IL-17A) and tumor necrosis factor-\u03b1 (TNF-\u03b1) induced NETosis in RA neutrophils.", "In turn, NETs significantly augmented inflammatory responses in RA and OA synovial fibroblasts, including induction of IL-6, IL-8, chemokines, and adhesion molecules.", "These observations implicate accelerated NETosis in RA pathogenesis, through externalization of citrullinated autoantigens and immunostimulatory molecules that may promote aberrant adaptive and innate immune responses in the joint and in the periphery, and perpetuate pathogenic mechanisms in this disease."]}