Intestinal inflammation observed in IL-2R/IL-2 mutant mice is associated with impaired intestinal T lymphopoiesis
Background & Aims: Although interleukin (IL)-2 −/− and IL-2Rα −/− mice develop inflammatory bowel disease, IL-2Rβ −/− animals are apparently free of gut pathology. Intraintestinal T lymphopoiesis is reported to be impaired in IL-2Rβ −/− mice; we have determined whether this characteristic correl...
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| Veröffentlicht in: | Gastroenterology (New York, N.Y. 1943) N.Y. 1943), 2000-05, Vol.118 (5), p.880-891 |
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| container_title | Gastroenterology (New York, N.Y. 1943) |
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| creator | Poussier ,‡,§, Philippe Ning, Terri Chen, Jun Banerjee ∥, Diponkar Julius §, Michael |
| description | Background & Aims: Although interleukin (IL)-2
−/− and IL-2Rα
−/− mice develop inflammatory bowel disease, IL-2Rβ
−/− animals are apparently free of gut pathology. Intraintestinal T lymphopoiesis is reported to be impaired in IL-2Rβ
−/− mice; we have determined whether this characteristic correlated with the apparent resistance of this mutant strain to intestinal inflammation. This led us to reassess intraintestinal T lymphopoiesis in these 3 mutant strains.
Methods: Intestinal histology and intraintestinal T lymphopoiesis were analyzed in unmanipulated mutant mice and in athymic and euthymic radiation chimeras reconstituted with bone marrow derived from IL-2
−/−, IL-2Rα
−/−, and IL-2Rβ
−/− donors.
Results: Intraintestinal T lymphopoiesis was ablated in the 3 mutant strains and was associated with cryptopatch abnormalities. The intestinal mucosa of mice reconstituted with lymphocytes from IL-2Rβ
−/− mice exhibited lesions of both the small and large bowel similar to those observed in the early stages of human gluten enteropathy and acute ulcerative colitis, respectively. Analysis of euthymic and athymic bone marrow radiation chimeras indicated that T cells located in the intestinal mucosa of unmanipulated IL-2
−/−, IL-2Rα
−/−, and IL-2Rβ
−/− mice are of thymic origin.
Conclusions: Null mutations at IL-2/IL-2Rα and β loci differentially affect intraintestinal and intrathymic T lymphopoiesis. These conditions are associated with lesions of intestinal inflammation that are mediated by thymus-derived T cells.
GASTROENTEROLOGY 2000;118:880-891 |
| doi_str_mv | 10.1016/S0016-5085(00)70174-0 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71066573</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0016508500701740</els_id><sourcerecordid>71066573</sourcerecordid><originalsourceid>FETCH-LOGICAL-c437t-d44ad2c5b95a7aba545501e8629a4d75e35ee8585789a3c102287ad93bb38b003</originalsourceid><addsrcrecordid>eNqFkN1rFDEQwIMo9lr9E5Q8iOjDtpPN5pJ9EilqDw6EWp_DbHaORjab7SbX0v_e3AfVt77MwMxvPvgx9k7AuQCxvPgFJVYKjPoE8FmD0E0FL9hCqNpUpVe_ZIsn5ISdpvQHAFppxGt2IkCbRhm9YHerMVPKfsSB-3EzYAiYfRx57BLN99SXKl-tq_r6Yhd52GYcMw_eEfeJY0rRecyFe_D5lvswoZ_3U09rb_jwGKbbOEVPyac37NUGh0Rvj_mM_f7-7ebyqlr__LG6_LquXCN1rvqmwb52qmsVauxQNUqBILOsW2x6rUgqIqOM0qZF6QTUtdHYt7LrpOkA5Bn7eNg7zfFuW56xwSdHw4AjxW2yWsByqbQsoDqAbo4pzbSx0-wDzo9WgN25tnvXdifSAti9a7s78P54YNsF6v-bOsgtwIcjgMnhsJlxdD7946RsDZiCfTlgVGzce5ptcp5GR30x6bLto3_mk78xJpsx</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>71066573</pqid></control><display><type>article</type><title>Intestinal inflammation observed in IL-2R/IL-2 mutant mice is associated with impaired intestinal T lymphopoiesis</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><source>Alma/SFX Local Collection</source><creator>Poussier ,‡,§, Philippe ; Ning, Terri ; Chen, Jun ; Banerjee ∥, Diponkar ; Julius §, Michael</creator><creatorcontrib>Poussier ,‡,§, Philippe ; Ning, Terri ; Chen, Jun ; Banerjee ∥, Diponkar ; Julius §, Michael</creatorcontrib><description>Background & Aims: Although interleukin (IL)-2
−/− and IL-2Rα
−/− mice develop inflammatory bowel disease, IL-2Rβ
−/− animals are apparently free of gut pathology. Intraintestinal T lymphopoiesis is reported to be impaired in IL-2Rβ
−/− mice; we have determined whether this characteristic correlated with the apparent resistance of this mutant strain to intestinal inflammation. This led us to reassess intraintestinal T lymphopoiesis in these 3 mutant strains.
Methods: Intestinal histology and intraintestinal T lymphopoiesis were analyzed in unmanipulated mutant mice and in athymic and euthymic radiation chimeras reconstituted with bone marrow derived from IL-2
−/−, IL-2Rα
−/−, and IL-2Rβ
−/− donors.
Results: Intraintestinal T lymphopoiesis was ablated in the 3 mutant strains and was associated with cryptopatch abnormalities. The intestinal mucosa of mice reconstituted with lymphocytes from IL-2Rβ
−/− mice exhibited lesions of both the small and large bowel similar to those observed in the early stages of human gluten enteropathy and acute ulcerative colitis, respectively. Analysis of euthymic and athymic bone marrow radiation chimeras indicated that T cells located in the intestinal mucosa of unmanipulated IL-2
−/−, IL-2Rα
−/−, and IL-2Rβ
−/− mice are of thymic origin.
Conclusions: Null mutations at IL-2/IL-2Rα and β loci differentially affect intraintestinal and intrathymic T lymphopoiesis. These conditions are associated with lesions of intestinal inflammation that are mediated by thymus-derived T cells.
GASTROENTEROLOGY 2000;118:880-891</description><identifier>ISSN: 0016-5085</identifier><identifier>EISSN: 1528-0012</identifier><identifier>DOI: 10.1016/S0016-5085(00)70174-0</identifier><identifier>PMID: 10784587</identifier><identifier>CODEN: GASTAB</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; CD4-Positive T-Lymphocytes - immunology ; CD4-Positive T-Lymphocytes - pathology ; Enterocolitis - genetics ; Enterocolitis - immunology ; Enterocolitis - pathology ; Flow Cytometry ; Fluorescent Antibody Technique ; Gastroenterology. Liver. Pancreas. Abdomen ; Interleukin-2 - deficiency ; Interleukin-2 - genetics ; Intestinal Mucosa - immunology ; Intestinal Mucosa - pathology ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Nude ; Other diseases. Semiology ; Phenotype ; Radiation Chimera ; Receptors, Interleukin-2 - deficiency ; Receptors, Interleukin-2 - genetics ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; T-Lymphocytes - immunology ; T-Lymphocytes - pathology ; Thymus Gland - immunology ; Thymus Gland - pathology</subject><ispartof>Gastroenterology (New York, N.Y. 1943), 2000-05, Vol.118 (5), p.880-891</ispartof><rights>2000 American Gastroenterological Association</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c437t-d44ad2c5b95a7aba545501e8629a4d75e35ee8585789a3c102287ad93bb38b003</citedby><cites>FETCH-LOGICAL-c437t-d44ad2c5b95a7aba545501e8629a4d75e35ee8585789a3c102287ad93bb38b003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0016508500701740$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1339808$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10784587$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Poussier ,‡,§, Philippe</creatorcontrib><creatorcontrib>Ning, Terri</creatorcontrib><creatorcontrib>Chen, Jun</creatorcontrib><creatorcontrib>Banerjee ∥, Diponkar</creatorcontrib><creatorcontrib>Julius §, Michael</creatorcontrib><title>Intestinal inflammation observed in IL-2R/IL-2 mutant mice is associated with impaired intestinal T lymphopoiesis</title><title>Gastroenterology (New York, N.Y. 1943)</title><addtitle>Gastroenterology</addtitle><description>Background & Aims: Although interleukin (IL)-2
−/− and IL-2Rα
−/− mice develop inflammatory bowel disease, IL-2Rβ
−/− animals are apparently free of gut pathology. Intraintestinal T lymphopoiesis is reported to be impaired in IL-2Rβ
−/− mice; we have determined whether this characteristic correlated with the apparent resistance of this mutant strain to intestinal inflammation. This led us to reassess intraintestinal T lymphopoiesis in these 3 mutant strains.
Methods: Intestinal histology and intraintestinal T lymphopoiesis were analyzed in unmanipulated mutant mice and in athymic and euthymic radiation chimeras reconstituted with bone marrow derived from IL-2
−/−, IL-2Rα
−/−, and IL-2Rβ
−/− donors.
Results: Intraintestinal T lymphopoiesis was ablated in the 3 mutant strains and was associated with cryptopatch abnormalities. The intestinal mucosa of mice reconstituted with lymphocytes from IL-2Rβ
−/− mice exhibited lesions of both the small and large bowel similar to those observed in the early stages of human gluten enteropathy and acute ulcerative colitis, respectively. Analysis of euthymic and athymic bone marrow radiation chimeras indicated that T cells located in the intestinal mucosa of unmanipulated IL-2
−/−, IL-2Rα
−/−, and IL-2Rβ
−/− mice are of thymic origin.
Conclusions: Null mutations at IL-2/IL-2Rα and β loci differentially affect intraintestinal and intrathymic T lymphopoiesis. These conditions are associated with lesions of intestinal inflammation that are mediated by thymus-derived T cells.
GASTROENTEROLOGY 2000;118:880-891</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD4-Positive T-Lymphocytes - pathology</subject><subject>Enterocolitis - genetics</subject><subject>Enterocolitis - immunology</subject><subject>Enterocolitis - pathology</subject><subject>Flow Cytometry</subject><subject>Fluorescent Antibody Technique</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Interleukin-2 - deficiency</subject><subject>Interleukin-2 - genetics</subject><subject>Intestinal Mucosa - immunology</subject><subject>Intestinal Mucosa - pathology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Nude</subject><subject>Other diseases. Semiology</subject><subject>Phenotype</subject><subject>Radiation Chimera</subject><subject>Receptors, Interleukin-2 - deficiency</subject><subject>Receptors, Interleukin-2 - genetics</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>T-Lymphocytes - immunology</subject><subject>T-Lymphocytes - pathology</subject><subject>Thymus Gland - immunology</subject><subject>Thymus Gland - pathology</subject><issn>0016-5085</issn><issn>1528-0012</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkN1rFDEQwIMo9lr9E5Q8iOjDtpPN5pJ9EilqDw6EWp_DbHaORjab7SbX0v_e3AfVt77MwMxvPvgx9k7AuQCxvPgFJVYKjPoE8FmD0E0FL9hCqNpUpVe_ZIsn5ISdpvQHAFppxGt2IkCbRhm9YHerMVPKfsSB-3EzYAiYfRx57BLN99SXKl-tq_r6Yhd52GYcMw_eEfeJY0rRecyFe_D5lvswoZ_3U09rb_jwGKbbOEVPyac37NUGh0Rvj_mM_f7-7ebyqlr__LG6_LquXCN1rvqmwb52qmsVauxQNUqBILOsW2x6rUgqIqOM0qZF6QTUtdHYt7LrpOkA5Bn7eNg7zfFuW56xwSdHw4AjxW2yWsByqbQsoDqAbo4pzbSx0-wDzo9WgN25tnvXdifSAti9a7s78P54YNsF6v-bOsgtwIcjgMnhsJlxdD7946RsDZiCfTlgVGzce5ptcp5GR30x6bLto3_mk78xJpsx</recordid><startdate>20000501</startdate><enddate>20000501</enddate><creator>Poussier ,‡,§, Philippe</creator><creator>Ning, Terri</creator><creator>Chen, Jun</creator><creator>Banerjee ∥, Diponkar</creator><creator>Julius §, Michael</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20000501</creationdate><title>Intestinal inflammation observed in IL-2R/IL-2 mutant mice is associated with impaired intestinal T lymphopoiesis</title><author>Poussier ,‡,§, Philippe ; Ning, Terri ; Chen, Jun ; Banerjee ∥, Diponkar ; Julius §, Michael</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c437t-d44ad2c5b95a7aba545501e8629a4d75e35ee8585789a3c102287ad93bb38b003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>CD4-Positive T-Lymphocytes - pathology</topic><topic>Enterocolitis - genetics</topic><topic>Enterocolitis - immunology</topic><topic>Enterocolitis - pathology</topic><topic>Flow Cytometry</topic><topic>Fluorescent Antibody Technique</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Interleukin-2 - deficiency</topic><topic>Interleukin-2 - genetics</topic><topic>Intestinal Mucosa - immunology</topic><topic>Intestinal Mucosa - pathology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Nude</topic><topic>Other diseases. Semiology</topic><topic>Phenotype</topic><topic>Radiation Chimera</topic><topic>Receptors, Interleukin-2 - deficiency</topic><topic>Receptors, Interleukin-2 - genetics</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>T-Lymphocytes - immunology</topic><topic>T-Lymphocytes - pathology</topic><topic>Thymus Gland - immunology</topic><topic>Thymus Gland - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Poussier ,‡,§, Philippe</creatorcontrib><creatorcontrib>Ning, Terri</creatorcontrib><creatorcontrib>Chen, Jun</creatorcontrib><creatorcontrib>Banerjee ∥, Diponkar</creatorcontrib><creatorcontrib>Julius §, Michael</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Poussier ,‡,§, Philippe</au><au>Ning, Terri</au><au>Chen, Jun</au><au>Banerjee ∥, Diponkar</au><au>Julius §, Michael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intestinal inflammation observed in IL-2R/IL-2 mutant mice is associated with impaired intestinal T lymphopoiesis</atitle><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle><addtitle>Gastroenterology</addtitle><date>2000-05-01</date><risdate>2000</risdate><volume>118</volume><issue>5</issue><spage>880</spage><epage>891</epage><pages>880-891</pages><issn>0016-5085</issn><eissn>1528-0012</eissn><coden>GASTAB</coden><abstract>Background & Aims: Although interleukin (IL)-2
−/− and IL-2Rα
−/− mice develop inflammatory bowel disease, IL-2Rβ
−/− animals are apparently free of gut pathology. Intraintestinal T lymphopoiesis is reported to be impaired in IL-2Rβ
−/− mice; we have determined whether this characteristic correlated with the apparent resistance of this mutant strain to intestinal inflammation. This led us to reassess intraintestinal T lymphopoiesis in these 3 mutant strains.
Methods: Intestinal histology and intraintestinal T lymphopoiesis were analyzed in unmanipulated mutant mice and in athymic and euthymic radiation chimeras reconstituted with bone marrow derived from IL-2
−/−, IL-2Rα
−/−, and IL-2Rβ
−/− donors.
Results: Intraintestinal T lymphopoiesis was ablated in the 3 mutant strains and was associated with cryptopatch abnormalities. The intestinal mucosa of mice reconstituted with lymphocytes from IL-2Rβ
−/− mice exhibited lesions of both the small and large bowel similar to those observed in the early stages of human gluten enteropathy and acute ulcerative colitis, respectively. Analysis of euthymic and athymic bone marrow radiation chimeras indicated that T cells located in the intestinal mucosa of unmanipulated IL-2
−/−, IL-2Rα
−/−, and IL-2Rβ
−/− mice are of thymic origin.
Conclusions: Null mutations at IL-2/IL-2Rα and β loci differentially affect intraintestinal and intrathymic T lymphopoiesis. These conditions are associated with lesions of intestinal inflammation that are mediated by thymus-derived T cells.
GASTROENTEROLOGY 2000;118:880-891</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>10784587</pmid><doi>10.1016/S0016-5085(00)70174-0</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Gastroenterology (New York, N.Y. 1943), 2000-05, Vol.118 (5), p.880-891 |
| issn | 0016-5085 1528-0012 |
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| source | MEDLINE; Elsevier ScienceDirect Journals; Alma/SFX Local Collection |
| subjects | Animals Biological and medical sciences CD4-Positive T-Lymphocytes - immunology CD4-Positive T-Lymphocytes - pathology Enterocolitis - genetics Enterocolitis - immunology Enterocolitis - pathology Flow Cytometry Fluorescent Antibody Technique Gastroenterology. Liver. Pancreas. Abdomen Interleukin-2 - deficiency Interleukin-2 - genetics Intestinal Mucosa - immunology Intestinal Mucosa - pathology Medical sciences Mice Mice, Inbred C57BL Mice, Nude Other diseases. Semiology Phenotype Radiation Chimera Receptors, Interleukin-2 - deficiency Receptors, Interleukin-2 - genetics Stomach. Duodenum. Small intestine. Colon. Rectum. Anus T-Lymphocytes - immunology T-Lymphocytes - pathology Thymus Gland - immunology Thymus Gland - pathology |
| title | Intestinal inflammation observed in IL-2R/IL-2 mutant mice is associated with impaired intestinal T lymphopoiesis |
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