| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-51 |
Sentence |
denotes |
MICL controls inflammation in rheumatoid arthritis. |
| T2 |
52-63 |
Sentence |
denotes |
BACKGROUND: |
| T3 |
64-202 |
Sentence |
denotes |
Myeloid inhibitory C-type lectin-like receptor (MICL, Clec12A) is a C-type lectin receptor (CLR) expressed predominantly by myeloid cells. |
| T4 |
203-285 |
Sentence |
denotes |
Previous studies have suggested that MICL is involved in controlling inflammation. |
| T5 |
286-296 |
Sentence |
denotes |
OBJECTIVE: |
| T6 |
297-381 |
Sentence |
denotes |
To determine the role of this CLR in inflammatory pathology using Clec12A(-/-) mice. |
| T7 |
382-390 |
Sentence |
denotes |
METHODS: |
| T8 |
391-524 |
Sentence |
denotes |
Clec12A(-/-) mice were generated commercially and primarily characterised using the collagen antibody-induced arthritis (CAIA) model. |
| T9 |
525-729 |
Sentence |
denotes |
Mechanisms and progress of disease were characterised by clinical scoring, histology, flow cytometry, irradiation bone-marrow chimera generation, administration of blocking antibodies and in vivo imaging. |
| T10 |
730-881 |
Sentence |
denotes |
Characterisation of MICL in patients with rheumatoid arthritis (RA) was determined by immunohistochemistry and single nucleotide polymorphism analysis. |
| T11 |
882-965 |
Sentence |
denotes |
Anti-MICL antibodies were detected in patient serum by ELISA and dot-blot analysis. |
| T12 |
966-1159 |
Sentence |
denotes |
RESULTS: MICL-deficient animals did not present with pan-immune dysfunction, but exhibited markedly exacerbated inflammation during CAIA, owing to the inappropriate activation of myeloid cells. |
| T13 |
1160-1314 |
Sentence |
denotes |
Polymorphisms of MICL were not associated with disease in patients with RA, but this CLR was the target of autoantibodies in a subset of patients with RA. |
| T14 |
1315-1412 |
Sentence |
denotes |
In wild-type mice the administration of such antibodies recapitulated the Clec12A(-/-) phenotype. |
| T15 |
1413-1553 |
Sentence |
denotes |
CONCLUSIONS: MICL plays an essential role in regulating inflammation during arthritis and is an autoantigen in a subset of patients with RA. |
| T16 |
1554-1769 |
Sentence |
denotes |
These data suggest an entirely new mechanism underlying RA pathogenesis, whereby the threshold of myeloid cell activation can be modulated by autoantibodies that bind to cell membrane-expressed inhibitory receptors. |
| T1 |
0-51 |
Sentence |
denotes |
MICL controls inflammation in rheumatoid arthritis. |
| T2 |
52-63 |
Sentence |
denotes |
BACKGROUND: |
| T3 |
64-202 |
Sentence |
denotes |
Myeloid inhibitory C-type lectin-like receptor (MICL, Clec12A) is a C-type lectin receptor (CLR) expressed predominantly by myeloid cells. |
| T4 |
203-285 |
Sentence |
denotes |
Previous studies have suggested that MICL is involved in controlling inflammation. |
| T5 |
286-296 |
Sentence |
denotes |
OBJECTIVE: |
| T6 |
297-381 |
Sentence |
denotes |
To determine the role of this CLR in inflammatory pathology using Clec12A(-/-) mice. |
| T7 |
382-390 |
Sentence |
denotes |
METHODS: |
| T8 |
391-524 |
Sentence |
denotes |
Clec12A(-/-) mice were generated commercially and primarily characterised using the collagen antibody-induced arthritis (CAIA) model. |
| T9 |
525-729 |
Sentence |
denotes |
Mechanisms and progress of disease were characterised by clinical scoring, histology, flow cytometry, irradiation bone-marrow chimera generation, administration of blocking antibodies and in vivo imaging. |
| T10 |
730-881 |
Sentence |
denotes |
Characterisation of MICL in patients with rheumatoid arthritis (RA) was determined by immunohistochemistry and single nucleotide polymorphism analysis. |
| T11 |
882-965 |
Sentence |
denotes |
Anti-MICL antibodies were detected in patient serum by ELISA and dot-blot analysis. |
| T12 |
966-1159 |
Sentence |
denotes |
RESULTS: MICL-deficient animals did not present with pan-immune dysfunction, but exhibited markedly exacerbated inflammation during CAIA, owing to the inappropriate activation of myeloid cells. |
| T13 |
1160-1314 |
Sentence |
denotes |
Polymorphisms of MICL were not associated with disease in patients with RA, but this CLR was the target of autoantibodies in a subset of patients with RA. |
| T14 |
1315-1412 |
Sentence |
denotes |
In wild-type mice the administration of such antibodies recapitulated the Clec12A(-/-) phenotype. |
| T15 |
1413-1553 |
Sentence |
denotes |
CONCLUSIONS: MICL plays an essential role in regulating inflammation during arthritis and is an autoantigen in a subset of patients with RA. |
| T16 |
1554-1769 |
Sentence |
denotes |
These data suggest an entirely new mechanism underlying RA pathogenesis, whereby the threshold of myeloid cell activation can be modulated by autoantibodies that bind to cell membrane-expressed inhibitory receptors. |