000			02873nam a2200301 4500
001			ESSALUD
005			20260805113858.0
007			ta
008			t pe ||||| |||| 00| 0 spa d
040			_aBMG
041			_aeng
100			_aGharahdaghi, Nima _eAutor _953934
245			_aInterleukin-10 autoantibodies and HLA-DRB1*01:03 in inflammatory bowel disease
300			_apáginas: 2212-2222
520			_aBackground: Neutralizing autoantibodies against interleukin-10 can result in a phenocopy of monogenic defects of interleukin-10 signaling in children and may be associated with inflammatory bowel disease (IBD). The allele HLA-DRB1*01:03 is the strongest genetic risk factor for ulcerative colitis. Methods: We used a cellular interleukin-10 reporter assay and a confirmatory competitive enzyme-linked immunosorbent assay to assess neutralizing interleukin-10 autoantibodies in serum samples obtained from patients with IBD in the Oxford and U.K. IBD BioResource cohorts and from persons without IBD (controls). An in vitro cytokine-release bioassay was performed in a subgroup of patients to assess interleukin-10, interleukin-23, interleukin-1β, tumor necrosis factor, and interleukin-6. We performed HLA association analysis using imputation and high-resolution sequencing. Results: Interleukin-10–neutralizing autoantibodies were detected in 173 of 4909 patients with IBD (3.5%; 95% confidence interval [CI], 3.0 to 4.1) and in none of 1006 controls (P<0.001). High anti–interleukin-10 activity in serum was associated with a reduction in detectable interleukin-10 and with an exaggerated proinflammatory cytokine response, consistent with functional neutralization of interleukin-10 signaling. Anti–interleukin-10 seropositivity was strongly associated with HLA-DRB1*01:03 on the basis of imputed data from the Oxford cohort (odds ratio, 50.0; 95% CI, 16.4 to 152.3; P=6.14×10−12) and the U.K. IBD BioResource cohort (odds ratio, 24.7; 95% CI, 14.5 to 42.1; P=6.20×10−32) and in a high-resolution sequencing analysis of data from the Oxford cohort (odds ratio, 29.5; 95% CI, 12.2 to 71.1; P=4.85×10−14). Conclusions: Neutralizing interleukin-10 autoantibodies were present in a subgroup of patients with IBD and were strongly associated with HLA-DRB1*01:03.
650			_aALERGIA _97055
650			_aENFERMEDAD AUTOINMUNE _953665
650			_aGENETICA _91105
650			_aGASTROENTEROLOGÍA _912562
650			_aENFERMEDAD INFLAMATORIA INTESTINAL _953935
700			_aYeh, Pai-Jui _953936
700			_aCerón-Gutiérrez, Lourdes _953937
700			_aGriffin, Helen _953938
700			_aGordon, Hannah _953939
700			_aJayamanne, Chamara _953940
773	0		_022717 _922641 _dMassachusetts NEJM Group _oNEJM008 _tThe New England Journal of Medicine _wESSALUD _x0028-4793
942			_cARTICULOS _e2026-08-03 _zSQB
999			_c22776 _d22776