Ontogeny and immunohistochemical localization of thymus-dependent and thymus-independent RT6+ cells in the rat.
Identifieur interne : 000E78 ( Ncbi/Merge ); précédent : 000E77; suivant : 000E79Ontogeny and immunohistochemical localization of thymus-dependent and thymus-independent RT6+ cells in the rat.
Auteurs : D. J. Waite ; M. C. Appel ; E. S. Handler ; J. P. Mordes ; A. A. Rossini ; D. L. GreinerSource :
- The American Journal of Pathology [ 0002-9440 ] ; 1996.
Abstract
RT6 is a cell surface alloantigen that identifies a regulatory subset of peripheral T cells in the rat. Diabetes-prone BB rats are deficient in peripheral RT6+ T cells and develop spontaneous autoimmune insulin-dependent diabetes mellitus. Diabetes-resistant BB rats have normal numbers of RT6+ T cells, and insulin-dependent diabetes mellitus can be induced in these animals by in vivo depletion of peripheral RT6+ cells. Athymic rats are also severely deficient in peripheral RT6+ T cells. Although very different with respect to the peripheral RT6+ cell compartment, normal, athymic, and diabetes-prone BB rats all generate RT6+ intestinal epithelial lymphocytes (IELs). The goal of these studies was to analyze the ontogeny of RT6+ IELs and peripheral lymphoid cells by in situ immunohistochemistry. We observed the following. 1) RT6+ IELs appear before alpha(beta) T-cell-receptor- expressing IELs in diabetes-prone BB, diabetes-resistant BB, and athymic WAG rats. 2) In vivo depletion of peripheral RT6+ T cells in diabetes-resistant BB rats using a cytotoxic monoclonal antibody is not accompanied by depletion of RT6+ IELs. 3) A population of RT6+ T-cell-receptor-negative IELs is present in normal, euthymic diabetes-resistant BB rats, constitutes a larger percentage of the euthymic but lymphopenic diabetes-prone BB rat IEL population, and is the predominant IEL phenotype in athymic WAG rats. These results suggest that RT6+ cells are composed of both thymus-dependent and thymus-independent cell subsets that have different developmental characteristics and may differ in function.
Url:
PubMed: 8669488
PubMed Central: 1861642
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<author><name sortKey="Handler, E S" sort="Handler, E S" uniqKey="Handler E" first="E. S." last="Handler">E. S. Handler</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Ontogeny and immunohistochemical localization of thymus-dependent and thymus-independent RT6+ cells in the rat.</title>
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<series><title level="j">The American Journal of Pathology</title>
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<front><div type="abstract" xml:lang="en"><p>RT6 is a cell surface alloantigen that identifies a regulatory subset of peripheral T cells in the rat. Diabetes-prone BB rats are deficient in peripheral RT6+ T cells and develop spontaneous autoimmune insulin-dependent diabetes mellitus. Diabetes-resistant BB rats have normal numbers of RT6+ T cells, and insulin-dependent diabetes mellitus can be induced in these animals by in vivo depletion of peripheral RT6+ cells. Athymic rats are also severely deficient in peripheral RT6+ T cells. Although very different with respect to the peripheral RT6+ cell compartment, normal, athymic, and diabetes-prone BB rats all generate RT6+ intestinal epithelial lymphocytes (IELs). The goal of these studies was to analyze the ontogeny of RT6+ IELs and peripheral lymphoid cells by in situ immunohistochemistry. We observed the following. 1) RT6+ IELs appear before alpha(beta) T-cell-receptor- expressing IELs in diabetes-prone BB, diabetes-resistant BB, and athymic WAG rats. 2) In vivo depletion of peripheral RT6+ T cells in diabetes-resistant BB rats using a cytotoxic monoclonal antibody is not accompanied by depletion of RT6+ IELs. 3) A population of RT6+ T-cell-receptor-negative IELs is present in normal, euthymic diabetes-resistant BB rats, constitutes a larger percentage of the euthymic but lymphopenic diabetes-prone BB rat IEL population, and is the predominant IEL phenotype in athymic WAG rats. These results suggest that RT6+ cells are composed of both thymus-dependent and thymus-independent cell subsets that have different developmental characteristics and may differ in function.</p>
<sec sec-type="scanned-figures"><title>Images</title>
<fig id="F1"><label>Figure 1</label>
<graphic xlink:href="amjpathol00042-0319-a" xlink:role="2046"></graphic>
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<fig id="F2"><label>Figure 2</label>
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<fig id="F3"><label>Figure 3</label>
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<fig id="F4"><label>Figure 4</label>
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<fig id="F5"><label>Figure 5</label>
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<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Am J Pathol</journal-id>
<journal-title>The American Journal of Pathology</journal-title>
<issn pub-type="ppub">0002-9440</issn>
<issn pub-type="epub">1525-2191</issn>
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<article-id pub-id-type="pmc">1861642</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject>
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<title-group><article-title>Ontogeny and immunohistochemical localization of thymus-dependent and thymus-independent RT6+ cells in the rat.</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Waite</surname>
<given-names>D. J.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Appel</surname>
<given-names>M. C.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Handler</surname>
<given-names>E. S.</given-names>
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<contrib contrib-type="author"><name><surname>Mordes</surname>
<given-names>J. P.</given-names>
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<contrib contrib-type="author"><name><surname>Rossini</surname>
<given-names>A. A.</given-names>
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<contrib contrib-type="author"><name><surname>Greiner</surname>
<given-names>D. L.</given-names>
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<aff>Department of Medicine, Diabetes Division, University of Massachusetts Medical Center, Worcester, Massachusetts 01605, USA.</aff>
<pub-date pub-type="ppub"><month>6</month>
<year>1996</year>
</pub-date>
<volume>148</volume>
<issue>6</issue>
<fpage>2043</fpage>
<lpage>2056</lpage>
<abstract><p>RT6 is a cell surface alloantigen that identifies a regulatory subset of peripheral T cells in the rat. Diabetes-prone BB rats are deficient in peripheral RT6+ T cells and develop spontaneous autoimmune insulin-dependent diabetes mellitus. Diabetes-resistant BB rats have normal numbers of RT6+ T cells, and insulin-dependent diabetes mellitus can be induced in these animals by in vivo depletion of peripheral RT6+ cells. Athymic rats are also severely deficient in peripheral RT6+ T cells. Although very different with respect to the peripheral RT6+ cell compartment, normal, athymic, and diabetes-prone BB rats all generate RT6+ intestinal epithelial lymphocytes (IELs). The goal of these studies was to analyze the ontogeny of RT6+ IELs and peripheral lymphoid cells by in situ immunohistochemistry. We observed the following. 1) RT6+ IELs appear before alpha(beta) T-cell-receptor- expressing IELs in diabetes-prone BB, diabetes-resistant BB, and athymic WAG rats. 2) In vivo depletion of peripheral RT6+ T cells in diabetes-resistant BB rats using a cytotoxic monoclonal antibody is not accompanied by depletion of RT6+ IELs. 3) A population of RT6+ T-cell-receptor-negative IELs is present in normal, euthymic diabetes-resistant BB rats, constitutes a larger percentage of the euthymic but lymphopenic diabetes-prone BB rat IEL population, and is the predominant IEL phenotype in athymic WAG rats. These results suggest that RT6+ cells are composed of both thymus-dependent and thymus-independent cell subsets that have different developmental characteristics and may differ in function.</p>
<sec sec-type="scanned-figures"><title>Images</title>
<fig id="F1"><label>Figure 1</label>
<graphic xlink:href="amjpathol00042-0319-a" xlink:role="2046"></graphic>
</fig>
<fig id="F2"><label>Figure 2</label>
<graphic xlink:href="amjpathol00042-0321-a" xlink:role="2048"></graphic>
</fig>
<fig id="F3"><label>Figure 3</label>
<graphic xlink:href="amjpathol00042-0323-a" xlink:role="2050"></graphic>
</fig>
<fig id="F4"><label>Figure 4</label>
<graphic xlink:href="amjpathol00042-0324-a" xlink:role="2051"></graphic>
</fig>
<fig id="F5"><label>Figure 5</label>
<graphic xlink:href="amjpathol00042-0325-a" xlink:role="2052"></graphic>
</fig>
<fig id="F6"><label>Figure 6</label>
<graphic xlink:href="amjpathol00042-0326-a" xlink:role="2053"></graphic>
</fig>
</sec>
</abstract>
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<name sortKey="Greiner, D L" sort="Greiner, D L" uniqKey="Greiner D" first="D. L." last="Greiner">D. L. Greiner</name>
<name sortKey="Handler, E S" sort="Handler, E S" uniqKey="Handler E" first="E. S." last="Handler">E. S. Handler</name>
<name sortKey="Mordes, J P" sort="Mordes, J P" uniqKey="Mordes J" first="J. P." last="Mordes">J. P. Mordes</name>
<name sortKey="Rossini, A A" sort="Rossini, A A" uniqKey="Rossini A" first="A. A." last="Rossini">A. A. Rossini</name>
<name sortKey="Waite, D J" sort="Waite, D J" uniqKey="Waite D" first="D. J." last="Waite">D. J. Waite</name>
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