1 tral stenosis, and Sir David Dundas on acute rheumatic carditis.

2  responses to cardiac myosin were similar in rheumatic carditis among a small sample of worldwide pop

3 ted with inflammatory heart diseases such as rheumatic carditis and myocarditis.

4 eripheral blood lymphocytes of patients with rheumatic carditis, and mAb 10.2.5, produced from a tons

5 hypothesis that cross-reactive antibodies in rheumatic carditis cause injury at the endothelium and u

6                               An analysis of rheumatic carditis in a Pacific Islander family confirme

7 f human cardiac myosin in the development of rheumatic carditis in humans.

8 ate that the pathogenic antibody response in rheumatic carditis may reflect the conversion of a T-cel

9 that anti-GlcNAc/anti-myosin mAb 3.B6 from a rheumatic carditis patient was cytotoxic for human endot

10 NAc, mimicking a subset of MAbs derived from rheumatic carditis patients that bind both myosin and st

11 ort suggests that cardiac myosin epitopes in rheumatic carditis target the S2 region of cardiac myosi

12 es are present in autoimmune myocarditis and rheumatic carditis, the purpose of the current study was

13 ocarditis; however, in the developing world, rheumatic carditis, Trypanosoma cruzi, and bacterial inf

14 in-specific human T cell clones derived from rheumatic carditis were cross-reactive with human cardia

15                    The anti-myosin mAbs from rheumatic carditis were found to react with specific pep

16 yosin and are similar among populations with rheumatic carditis worldwide, regardless of the infectin