Authors: Lynne E Nield Ingo von Both Najla Popel Kate Strachan Cedric Manlhiot Patrick Shannon Brian W McCrindle Adelle Atkinson Steven E S Miner Edgar T Jaeggi Glenn P Taylor
Publish Date: 2015/10/20
Volume: 37, Issue: 2, Pages: 353-363
Abstract
The etiology of idiopathic dilated cardiomyopathy iDCM remains unknown Immune therapies have improved outcome in fetuses with DCM born to mothers with autoimmune disease aDCM The purpose of this retrospective study was to compare the myocardial B and T cell profiles in fetuses and neonates with idiopathic DCM iDCM versus autoimmunemediated DCM aDCM and to describe the normal cell maturation within the human fetal myocardium Of 60 fetal autopsy cases identified from institutional databases 10 had aDCM 18–38 weeks 12 iDCM 19–37 weeks and 38 had normal hearts 11–40 weeks Paraffinembedded myocardium sections were stained for all lymphocyte CD45 B cells CD20 CD79a T cells CD3 CD4 CD7 CD8 and monocyte CD68 surface markers Two independent blinded cell counts were performed Normal hearts expressed all B and T cell markers in a bimodal fashion with peaks at 22 and 37 weeks of gestation The aDCM cohort was most distinct from normal hearts with less overall T cell markers EST −91 26 cells/mm2 p = 0001 CD4 EST −20 06 p = 0001 CD3 EST −39 10 p 0001 CD7 EST −30 11 p = 001 overall B cell markers EST −49 18 p = 001 and CD79a counts EST −23 09 p = 001 The iDCM group had less overall B cell markers EST −40 18 p = 003 and CD79a EST −17 09 p = 005 but no difference in T cell markers Autoimmunemediated DCM fetuses have less B and T cell markers whereas iDCM fetuses have less B cell markers compared with normal fetal hearts The fetal immune system may play a role in the normal development of the heart and evolution of dilated cardiomyopathy
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