Dependence of Thymus Development on Derivatives of the Neural Crest

Bockman, Dale E.; Kirby, Margaret L.

doi:10.1126/science.6606851

Cited by 424 publications

(178 citation statements)

References 20 publications

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“…Moreover, 6AA anomalies were induced by large ablations that included the arch 6 region. The high incidence of 3AA anomalies in the arch 4 and arch 4-6 groups could be explained by scanning electron microscopic findings in another study, in which both the third and the fourth pharyngeal arches were hypoplastic in many of the incubation day 3 chick embryos after arch [4][5][6] …”

Section: Discussionmentioning

confidence: 99%

Pathogenesis of persistent truncus arteriosus and dextroposed aorta in the chick embryo after neural crest ablation.

Nishibatake¹,

Kirby²,

Mierop³

1987

Circulation

243

139

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To investigate the contribution of cranial neural crest cells to the developing cardiovascular system in the chick embryo, cauterization of various regions of cranial neural crest was performed. Five regions may be distinguished, each of which contributes mesenchyme to pharyngeal (branchial) arches 1 through 4 and 6. Ablation of arch 3, 4, and 6 regions resulted in a high incidence of persistent truncus arteriosus (PTA) associated with anomalies of the aortic arch. Dextroposed aorta (DPA) or anomalies of the inflow tract were found in all ablation groups. Although anomalies of the aortic arch arteries were induced in all ablation groups and were usually associated with intracardiac anomalies, those of the third and right fourth aortic arch were most frequent in the arch 4 and arch 4 + 6 groups. Anomalies of the sixth aortic arch were most frequent after extensive ablations that included the arch 6 region. We speculate that PTA is a direct result of the decreased population of mesenchymal cells derived from the arch 3 through 6 neural crest regions. DPA or anomalies of the inflow tract may be related to altered hemodynamics due to anomalies induced by neural crest ablation. Anomalies of the aortic arch arteries may be caused by either the direct or indirect process. Circulation 75, No. 1, 255-264, 1987. IT HAS BEEN SHOWN in quail-chick chimeras that the cranial neural crest supplies ectomesenchymal cells to the pharyngeal arches, which contain the aortic arch arteries.1 Moreover, cranial neural crest cells extending from the auditory placode to somite 3 migrate to the outflow tract of the heart to participate in aorticopulmonary and truncal septation in the chick embryo.2 Surgical removal of these premigratory cells results in a high incidence of conotruncal anomalies, which include persistent truncus arteriosus (PTA) and doubleoutlet right ventricle (DORV)34 in combination with hypoplasia or absence of pharyngeal pouch derivatives, i.e., thymus and parathyroid glands.5 These anomalies induced by ablation of cranial neural crest have morphologic features that resemble those of the DiGeorge syndrome in man.DiGeorge syndrome in man is associated with interrupted aortic arch type B, PTA, and tetralogy of Fal-

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Section: Discussionmentioning

confidence: 99%

Pathogenesis of persistent truncus arteriosus and dextroposed aorta in the chick embryo after neural crest ablation.

Nishibatake¹,

Kirby²,

Mierop³

1987

Circulation

243

139

View full text Add to dashboard Cite

show abstract

“…Hence, the thymus, parathyroid, and thyroid glands, all of which obtain their stroma from neural crest in the pharyngeal arches are affected. 20 The neural crest migrating into arches 1 and 2, that will develop into the lower face and upper neck, is cranial to the cardiac region of neural crest13; thus, facial structures are not usually affected by cardiac neural crest removal.…”

Section: Neural Crest-related Malforznationsmentioning

confidence: 99%

Role of neural crest in congenital heart disease.

1990

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“…The thymic primordium of mice arises bilaterally at day 10 of gestation (E10) 4 by fusion of the third pouch endoderm with ectoderm from the corresponding branchial clefts. The two tissues are separated by a thin layer of mesenchyme originating from the cephalic neural crest (1). While the relative contribution of each germ layer to the mature thymic epithelial compartment remains to be determined, a small subpopulation of epithelial cells has been characterized that represents a common precursor cell for mature cortical and medullary epithelium (2,3).…”

mentioning

confidence: 99%

Normal Thymic Architecture and Negative Selection Are Associated with Aire Expression, the Gene Defective in the Autoimmune-Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy (APECED)

Žuklys

Balc̆iūnaite

Agarwal

et al. 2000

The Journal of Immunology

234

159

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T cell development is tightly controlled by thymic stromal cells. Alterations in stromal architecture affect T cell maturation and the development of self-tolerance. The monogenic autoimmune syndrome APECED (autoimmune-polyendocrinopathy-candidiasis-ectodermal dystrophy) is characterized by the loss of self-tolerance to multiple organs. Although mutations in the autoimmune regulator (AIRE) gene are responsible for this disease, the function of AIRE is not known. Here we report on the spatial and temporal pattern of murine Aire expression during thymic ontogeny and T cell selection. Early during development, thymic Aire transcription is critically dependent on RelB and occurs in epithelial cells in response to lymphocyte-mediated signals. In adult tissue, Aire expression is confined to the medulla and the corticomedullary junction, where it is modulated by thymocytes undergoing negative selection. Aire may determine thymic stromal organization and with it the induction of self-tolerance.

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Dependence of Thymus Development on Derivatives of the Neural Crest

Cited by 424 publications

References 20 publications

Pathogenesis of persistent truncus arteriosus and dextroposed aorta in the chick embryo after neural crest ablation.

Pathogenesis of persistent truncus arteriosus and dextroposed aorta in the chick embryo after neural crest ablation.

Role of neural crest in congenital heart disease.

Normal Thymic Architecture and Negative Selection Are Associated with Aire Expression, the Gene Defective in the Autoimmune-Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy (APECED)

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