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rdf:type |
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lifeskim:mentions |
umls-concept:C0020962,
umls-concept:C0026809,
umls-concept:C0205307,
umls-concept:C0208973,
umls-concept:C0439660,
umls-concept:C0443146,
umls-concept:C0599883,
umls-concept:C1280500,
umls-concept:C1517892,
umls-concept:C1527180,
umls-concept:C1704666
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pubmed:issue |
2
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pubmed:dateCreated |
1989-12-13
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pubmed:abstractText |
The influence of sex steroids on cutaneous delayed-type hypersensitivity (DTH) and antibody responses to oxazolone (OXA) in autoimmune and normal mouse strains has been investigated. The results show that: (i) treatment with 17 beta-oestradiol (E2) suppresses DTH responses and stimulates antibody responses in MRL, B6 and C3H mice, suppresses DTH in DBA/1 mice, while having no effects on DTH or antibody responses in BALB/c and NFR/N mice. (ii) Treatment with testosterone suppresses the antibody response in all studied strains (MRL, B6, BALB/c and DBA/1) while down-regulating the DTH response only in MRL and B6 but not in BALB/c or DBA/1. (iii) Neither the lympho-proliferative (lpr) gene, which accelerates autoimmune disease, nor the H-2 genes seem to be directly related to the effects of sex hormones on the immune system. (iv) Susceptibility to oestrogen- and testosterone-mediated suppression of DTH but not oestrogen-mediated enhancement of antibody response are inherited as dominant traits. The results are discussed in the context of certain autoimmune diseases known to be influenced by sex hormone manipulations.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-13936595,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-14816426,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-308087,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-3372993,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-3485156,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-3491052,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-3501349,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-3871614,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-4678209,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-4797651,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-508371,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-508372,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-6126710,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-6165672,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-6368687,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-6607806,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-722243,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2807378-926210
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0019-2805
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
68
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
209-14
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:2807378-Animals,
pubmed-meshheading:2807378-Antigen-Antibody Reactions,
pubmed-meshheading:2807378-Autoimmune Diseases,
pubmed-meshheading:2807378-Estradiol,
pubmed-meshheading:2807378-Female,
pubmed-meshheading:2807378-Genes, Dominant,
pubmed-meshheading:2807378-Hypersensitivity, Delayed,
pubmed-meshheading:2807378-Immunoglobulin G,
pubmed-meshheading:2807378-Lymphocyte Activation,
pubmed-meshheading:2807378-Male,
pubmed-meshheading:2807378-Mice,
pubmed-meshheading:2807378-Mice, Inbred Strains,
pubmed-meshheading:2807378-Oxazoles,
pubmed-meshheading:2807378-Oxazolone,
pubmed-meshheading:2807378-Testosterone
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pubmed:year |
1989
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pubmed:articleTitle |
Oestradiol- and testosterone-mediated effects on the immune system in normal and autoimmune mice are genetically linked and inherited as dominant traits.
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pubmed:affiliation |
Department of Medical Microbiology, University of Göteborg, Sweden.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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