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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1991-7-12
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pubmed:abstractText |
The Leu-8 membrane glycoprotein is the primate homologue of the murine MEL-14 peripheral lymph node homing receptor and is expressed on a majority of circulating lymphocytes but on few lymphocytes in the intestinal lamina propria. To examine the mechanisms regulating expression of the Leu-8-molecule on lymphocytes in different tissue sites, studies of Leu-8 membrane antigen expression, Leu-8 messenger RNA, and the Leu-8 gene were performed using normal human and nonhuman primate lymphocytes. Activation of resting peripheral blood lymphocytes caused a rapid decrease in membrane Leu-8 expression, a more gradual decrease in Leu-8 messenger RNA, and an increase in expression of interleukin 2 and interleukin 2 receptor messenger RNA. However, the down regulation of Leu-8 expression during activation was reversible because both membrane Leu-8 antigen and Leu-8 messenger RNA were reexpressed after 5 days of culture. Leu-8 messenger RNA was present in lymphocytes isolated from peripheral blood, spleen, and, particularly, mesenteric lymph node, but intestinal lamina propria lymphocytes contained very low levels of Leu-8 messenger RNA. The absence of Leu-8 messenger RNA in intestinal lymphocytes and circulating Leu-8 negative lymphocytes was not caused by recent activation in vivo because these cells did not have detectable interleukin 2 messenger RNA, and intestinal lymphocytes did not express Leu-8 after culture in vitro. Phorbol myristate acetate was found to be a strong inducer of Leu-8 messenger RNA in Leu-8-positive lymphocytes; however, phorbol myristate acetate did not induce membrane Leu-8 expression or Leu-8 messenger RNA in lamina propria lymphocytes. Leu-8-negative lymphocytes in peripheral blood or lamina propria did not have evidence of deletion or rearrangement of the Leu-8 gene. Leu-8-positive Jurkat cells and peripheral blood lymphocytes and Leu-8-negative peripheral blood and intestinal lymphocytes had partial methylation of an Msp I site in proximity to the Leu-8 gene, suggesting that in Leu-8-negative lymphocytes, the Leu-8 gene previously was transcriptionally active. In summary, these studies demonstrate that intestinal lamina propria lymphocytes have the same characteristics as circulating Leu-8-negative lymphocytes with respect to their state of activation and inability to express the Leu-8 antigen. The results suggest that the majority of lymphocytes that migrate to the intestinal lamina propria are derived from the subpopulation of circulating Leu-8-negative lymphocytes.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Lymphocyte Homing,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0016-5085
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
101
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
90-9
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:2044931-Animals,
pubmed-meshheading:2044931-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:2044931-Cell Line,
pubmed-meshheading:2044931-Down-Regulation,
pubmed-meshheading:2044931-Gene Expression Regulation,
pubmed-meshheading:2044931-Humans,
pubmed-meshheading:2044931-Intestinal Mucosa,
pubmed-meshheading:2044931-Lymphocyte Activation,
pubmed-meshheading:2044931-Lymphocytes,
pubmed-meshheading:2044931-RNA, Messenger,
pubmed-meshheading:2044931-Receptors, Lymphocyte Homing,
pubmed-meshheading:2044931-Tetradecanoylphorbol Acetate,
pubmed-meshheading:2044931-Time Factors
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pubmed:year |
1991
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pubmed:articleTitle |
Lamina propria lymphocytes are derived from circulating cells that lack the Leu-8 lymph node homing receptor.
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pubmed:affiliation |
Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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