{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/20750"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/20750","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"The effects of vitamin A deficiency on the immune system in a murine model of systemic lupus erythematosus","abstract":"The objectives of the present study were to investigate the effects of vitamin A deficiency on the onset and progression of systemic lupus erythematosus (SLE), using the murine model, MRL/MPJ-lpr/lpr (MRL/l) mice in comparison with MRL/MP-+/+ (+/+) mice, and to postulate a possible mechanism. In Study I, sixty weanling female four week old MRL/l mice were randomly assigned to either the vitamin A-deficient (A-), A-sufficient (A+), and A-sufficient diet/feed restricted (DR) groups. In Study II fifty-eight same-age and -sex MRL/l mice were randomly assigned to either the A$-$ or A+ groups, while twenty-four +/+ mice, of the same sex and age range as MRL/l, were assigned to the normal control group (+/+ group). The results of both studies showed that vitamin A deficiency had a significant effect on preventing the MRL/l mice body weight loss due to the progression of SLE. Vitamin A deficiency also tended to suppress the abnormal enlargement of the thymus and spleen due to massive proliferation of abnormal T cells in MRL/l mice. The results of in vitro splenocyte proliferation tests indicate that vitamin A deficiency decreased the proportion of abnormal T and hypersecreation B cells so that the normal T and B cell ratio increased and was closer to the +/+ group in MRL/l mice. The results from Study II strongly suggested that the above beneficial effects of vitamin A deficiency were related to an increased expression of interleukin-2 (IL-2) receptor on the surface of the MRL/l mouse splenocytes, which resulted in an increased proliferation of normal T and B cells. To summarize, vitamin A deficiency decreases the overall progression of SLE in MRL/l mice. The mechanism includes an increased activity of suppressor T cells and an increased expression of IL-2 receptors on the surface of the splenocytes.","abstract_html":"The objectives of the present study were to investigate the effects of vitamin A deficiency on the onset and progression of systemic lupus erythematosus (SLE), using the murine model, MRL/MPJ-lpr/lpr (MRL/l) mice in comparison with MRL/MP-+/+ (+/+) mice, and to postulate a possible mechanism. In Study I, sixty weanling female four week old MRL/l mice were randomly assigned to either the vitamin A-deficient (A-), A-sufficient (A+), and A-sufficient diet/feed restricted (DR) groups. In Study II fifty-eight same-age and -sex MRL/l mice were randomly assigned to either the A$-$ or A+ groups, while twenty-four +/+ mice, of the same sex and age range as MRL/l, were assigned to the normal control group (+/+ group). The results of both studies showed that vitamin A deficiency had a significant effect on preventing the MRL/l mice body weight loss due to the progression of SLE. Vitamin A deficiency also tended to suppress the abnormal enlargement of the thymus and spleen due to massive proliferation of abnormal T cells in MRL/l mice. The results of in vitro splenocyte proliferation tests indicate that vitamin A deficiency decreased the proportion of abnormal T and hypersecreation B cells so that the normal T and B cell ratio increased and was closer to the +/+ group in MRL/l mice. The results from Study II strongly suggested that the above beneficial effects of vitamin A deficiency were related to an increased expression of interleukin-2 (IL-2) receptor on the surface of the MRL/l mouse splenocytes, which resulted in an increased proliferation of normal T and B cells. To summarize, vitamin A deficiency decreases the overall progression of SLE in MRL/l mice. The mechanism includes an increased activity of suppressor T cells and an increased expression of IL-2 receptors on the surface of the splenocytes.","abstract_has_math":true,"creators":["Liao, C. Hua"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Human and Community Development","degree_department":null,"school":null,"contributors":["Klein, Barbara P."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2011,"date_issued":"2011-05-07T12:48:11Z","date_published":"2011-05-07T12:48:11Z","updated_at":"2026-07-22T22:25:16Z","subjects":["Health Sciences, Nutrition","Health Sciences, Immunology","Biology, Cell"],"languages":["eng"],"rights":["Copyright 1993 Liao, C. Hua"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9314904","(UMI)AAI9314904"],"render_values":[{"text":"AAI9314904","href":null,"code":true},{"text":"(UMI)AAI9314904","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/20750","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Klein, Barbara P."]},{"key":"dc:creator","label":"Author","values":["Liao, C. 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Hua"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9314904","(UMI)AAI9314904","http://hdl.handle.net/2142/20750"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["The objectives of the present study were to investigate the effects of vitamin A deficiency on the onset and progression of systemic lupus erythematosus (SLE), using the murine model, MRL/MPJ-lpr/lpr (MRL/l) mice in comparison with MRL/MP-+/+ (+/+) mice, and to postulate a possible mechanism. In Study I, sixty weanling female four week old MRL/l mice were randomly assigned to either the vitamin A-deficient (A-), A-sufficient (A+), and A-sufficient diet/feed restricted (DR) groups. In Study II fifty-eight same-age and -sex MRL/l mice were randomly assigned to either the A$-$ or A+ groups, while twenty-four +/+ mice, of the same sex and age range as MRL/l, were assigned to the normal control group (+/+ group). The results of both studies showed that vitamin A deficiency had a significant effect on preventing the MRL/l mice body weight loss due to the progression of SLE. Vitamin A deficiency also tended to suppress the abnormal enlargement of the thymus and spleen due to massive proliferation of abnormal T cells in MRL/l mice. The results of in vitro splenocyte proliferation tests indicate that vitamin A deficiency decreased the proportion of abnormal T and hypersecreation B cells so that the normal T and B cell ratio increased and was closer to the +/+ group in MRL/l mice. The results from Study II strongly suggested that the above beneficial effects of vitamin A deficiency were related to an increased expression of interleukin-2 (IL-2) receptor on the surface of the MRL/l mouse splenocytes, which resulted in an increased proliferation of normal T and B cells. To summarize, vitamin A deficiency decreases the overall progression of SLE in MRL/l mice. The mechanism includes an increased activity of suppressor T cells and an increased expression of IL-2 receptors on the surface of the splenocytes.","Made available in DSpace on 2011-05-07T12:48:11Z (GMT). No. of bitstreams: 2 license.txt: 4922 bytes, checksum: 910b249b4beec47e7ab768910c8f966f (MD5) 9314904.pdf: 3721577 bytes, checksum: 10e619c55e9f06cb83fbd11b4bc5f232 (MD5) Previous issue date: 1993","Item marked as restricted to the 'UIUC Users [automated]' Group (id=2) by Howard Ding (hding2@illinois.edu) on 2011-05-07T14:46:01Z Item is restricted indefinitely.","Restriction data tranferred 2014-07-01T11:20:30-05:00 Original Data Group with Access UIUC Users [automated] Release Date: none Reason: ETDs are only available to UIUC Users without author permission","ETDs are only available to UIUC Users without author permission","U of I Only"]},{"key":"dc:title","label":"Title","values":["The effects of vitamin A deficiency on the immune system in a murine model of systemic lupus erythematosus"]}]}],"canonical_facts":{"dc:contributor":["Klein, Barbara P."],"dc:creator":["Liao, C. Hua"],"dc:date":["2011-05-07T12:48:11Z","10000-01-01","1993"],"dc:description":["The objectives of the present study were to investigate the effects of vitamin A deficiency on the onset and progression of systemic lupus erythematosus (SLE), using the murine model, MRL/MPJ-lpr/lpr (MRL/l) mice in comparison with MRL/MP-+/+ (+/+) mice, and to postulate a possible mechanism. In Study I, sixty weanling female four week old MRL/l mice were randomly assigned to either the vitamin A-deficient (A-), A-sufficient (A+), and A-sufficient diet/feed restricted (DR) groups. In Study II fifty-eight same-age and -sex MRL/l mice were randomly assigned to either the A$-$ or A+ groups, while twenty-four +/+ mice, of the same sex and age range as MRL/l, were assigned to the normal control group (+/+ group). The results of both studies showed that vitamin A deficiency had a significant effect on preventing the MRL/l mice body weight loss due to the progression of SLE. Vitamin A deficiency also tended to suppress the abnormal enlargement of the thymus and spleen due to massive proliferation of abnormal T cells in MRL/l mice. The results of in vitro splenocyte proliferation tests indicate that vitamin A deficiency decreased the proportion of abnormal T and hypersecreation B cells so that the normal T and B cell ratio increased and was closer to the +/+ group in MRL/l mice. The results from Study II strongly suggested that the above beneficial effects of vitamin A deficiency were related to an increased expression of interleukin-2 (IL-2) receptor on the surface of the MRL/l mouse splenocytes, which resulted in an increased proliferation of normal T and B cells. To summarize, vitamin A deficiency decreases the overall progression of SLE in MRL/l mice. The mechanism includes an increased activity of suppressor T cells and an increased expression of IL-2 receptors on the surface of the splenocytes.","Made available in DSpace on 2011-05-07T12:48:11Z (GMT). No. of bitstreams: 2 license.txt: 4922 bytes, checksum: 910b249b4beec47e7ab768910c8f966f (MD5) 9314904.pdf: 3721577 bytes, checksum: 10e619c55e9f06cb83fbd11b4bc5f232 (MD5) Previous issue date: 1993","Item marked as restricted to the 'UIUC Users [automated]' Group (id=2) by Howard Ding (hding2@illinois.edu) on 2011-05-07T14:46:01Z Item is restricted indefinitely.","Restriction data tranferred 2014-07-01T11:20:30-05:00 Original Data Group with Access UIUC Users [automated] Release Date: none Reason: ETDs are only available to UIUC Users without author permission","ETDs are only available to UIUC Users without author permission","U of I Only"],"dc:identifier":["AAI9314904","(UMI)AAI9314904","http://hdl.handle.net/2142/20750"],"dc:language":["eng"],"dc:rights":["Copyright 1993 Liao, C. Hua"],"dc:subject":["Health Sciences, Nutrition","Health Sciences, Immunology","Biology, Cell"],"dc:title":["The effects of vitamin A deficiency on the immune system in a murine model of systemic lupus erythematosus"],"dc:type":["text"],"thesis:degree_discipline":["Human and Community Development"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Ph.D."],"thesis:institution_name":["University of Illinois at Urbana-Champaign"]},"updated_at":"2026-07-22T22:25:16Z"}