Chimerism in children with juvenile dermatomyositis

Reed, Ann M.; Picornell, Yoana; Harwood, Aaron; Kredich, Deborah W.

doi:10.1016/s0140-6736(00)03500-5

Cited by 178 publications

(117 citation statements)

References 3 publications

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“…48 Similarly, using gender specific FISH, Reed et al observed the presence of maternal Mc among PBMC in 11 of 15 male children affected with juvenile dermatomyositis, compared to 5 of 17 healthy controls and in muscle tissues in 12 of 15 compared to 2 of 10 unrelated controls. 60 This finding was also confirmed by Artlett et al by HLA specific PCR from blood. 61 Interestingly, in a study of twins born from a mother affected with MS, only the twin affected with MS presented high levels of maternal Mc.…”

Section: Maternal Microchimerism May Trigger Allogeneic Responsessupporting

confidence: 66%

Can maternal microchimeric cells influence the fetal response toward self antigens?

Lévêque

Khosrotehrani

2011

Chimerism

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Section: Maternal Microchimerism May Trigger Allogeneic Responsessupporting

confidence: 66%

Can maternal microchimeric cells influence the fetal response toward self antigens?

Lévêque

Khosrotehrani

2011

Chimerism

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“…Investigators in our group previously demonstrated maternal chimerism in juvenile DM (24,39) and other autoimmune disorders. In maternal chimerism, akin to graft-versus-host disease, it is thought that maternally derived T and B cells could be reactive with the host (the child with juvenile DM) (45).…”

Section: Discussionmentioning

confidence: 91%

“…Microchimerism. Investigators in our group have reported that juvenile DM is characterized by microchimerism, in which maternal cells can be identified in the inflammatory lesions in the muscle as well as in circulating leukocytes (39). Microchimerism has been postulated to be one of the driving forces of autoimmunity in juvenile DM (39,40).…”

mentioning

confidence: 96%

Extranodal lymphoid microstructures in inflamed muscle and disease severity of new‐onset juvenile dermatomyositis

Padilla¹,

Vallejo²,

Lacomis³

et al. 2009

Arthritis & Rheumatism

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Objective. Juvenile dermatomyositis (DM) is an autoimmune disease of childhood characterized by lesions in skin and muscle that are populated by plasmacytoid dendritic cells (PDCs) and lymphocyte infiltrates. We undertook this study to examine the cellular composition, organization, and molecular milieu of the cellular infiltrates in muscle in juvenile DM and to correlate the infiltrates with clinical disease manifestations.Methods. Since PDCs and lymphocyte foci express CCL19 and CCL21, we investigated for in situ formation of lymphoid microstructures that could be sites of extranodal immune activation.Results. Analyses of muscle biopsy samples from children with new-onset juvenile DM showed 3 categories of lesions: diffuse infiltrates, lymphocytic aggregates lacking follicle-like organization, and follicle-like structures. The last of these exhibited elements of classic lymphoid follicles, including networks of follicular dendritic cells and high endothelial venules. They also expressed high levels of CXCL13 and lymphotoxins known to support lymphoid organogenesis. There were also resident naive CD45RA؉ T cells and maternally derived B cells and PDCs. Patients with diffuse infiltrates or lymphocytic aggregates were responsive to standard therapy with steroids and methotrexate, but those with follicle-like structures tended to have severe disease that required additional agents such as intravenous Ig or rituximab.Conclusion. These data suggest that lymphoneogenesis is a component of the early disease process in juvenile DM. Ectopic lymphoid structures could indicate a severe course of disease; their early detection could be a tool for disease management.

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“…As suggested in studies of dermatomyositis (13), one consideration is that maternal microchimerism might affect a mother's progeny through anti-fetal alloreactive T cell responses. Female cells (presumed to be maternal) have been described in the tissues of male neonates (14), and an increase in the number of female cells has been reported in the muscle tissues of children with dermatomyositis (15) or idiopathic myositis (16). We recently identified maternal (female) cardiac myocytes in the heart muscle and atrioventricular node of male infants who died of heart block associated with neonatal lupus syndrome (17), suggesting the additional possibility that maternal cells could potentially be tissue targets of immune response (or, alternatively, could be involved in tissue repair).…”

Section: Discussionmentioning

confidence: 99%

Maternal HLA class II compatibility in men with systemic lupus erythematosus

Stevens

Tsao

Hahn

et al. 2005

Arthritis & Rheumatism

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Objective. Maternal-fetal cell transfer during pregnancy can lead to long-lasting microchimerism, which raises the question of whether microchimerism sometimes contributes to autoimmune disease later in life. In an experimental model, transfusion of parental lymphocytes homozygous for major histocompatibility complex alleles results in systemic lupus erythematosus (SLE). We identified male patients with SLE and healthy male subjects and their mothers in order to investigate the mother-son HLA relationship in SLE risk. Male subjects were selected in order to avoid confounding due to fetal microchimerism, which may occur in women.Methods. HLA genotyping for DRB1, DQA1, and DQB1 was conducted for sons and their mothers. Thirty men with SLE and their mothers were compared with 76 healthy men and their mothers.Results. Sons with SLE were HLA-identical with their mothers (bidirectionally compatible) for the basic HLA-DRB1 groups encoded by DRB1*01 through DRB1*14 more often than were healthy sons (odds ratio [OR] 5.0, P ‫؍‬ 0.006). Each DRB1 group contains multiple allelic variants; male patients with SLE and their mothers often were identical for both DRB1 allelic variants (OR 3.2, P ‫؍‬ 0.08). For DQA1 and DQB1, the ORs were 2.3 (P ‫؍‬ 0.08) and 2.0 (P ‫؍‬ 0.21), respectively. When analysis was limited to male subjects with SLEassociated HLA genes (encoding HLA-DR2 or HLA-DR3), the differences further increased for DRB1 basic groups (OR 7.2, P ‫؍‬ 0.01), DRB1 alleles (OR 15.0, P ‫؍‬ 0.018), DQA1 6.4 (P ‫؍‬ 0.006), and DQB1 (OR 5.7, P ‫؍‬ 0.027). No increase in (unidirectional) compatibility of the mother from the son's perspective was observed at any locus.Conclusion. We observed increased bidirectional HLA class II compatibility of male SLE patients and their mothers compared with healthy men and their mothers. This observation implies that maternal microchimerism could sometimes be involved in SLE and therefore merits further investigation.

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Chimerism in children with juvenile dermatomyositis

Cited by 178 publications

References 3 publications

Can maternal microchimeric cells influence the fetal response toward self antigens?

Can maternal microchimeric cells influence the fetal response toward self antigens?

Extranodal lymphoid microstructures in inflamed muscle and disease severity of new‐onset juvenile dermatomyositis

Maternal HLA class II compatibility in men with systemic lupus erythematosus

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