{"id":{"repo_id":"vt","oai_identifier":"oai:vtechworks.lib.vt.edu:10919/41612"},"canonical_url":"https://search.dev.ndltd.org/etd/vt/oai:vtechworks.lib.vt.edu:10919/41612","repository":{"repo_id":"vt","name":"Virginia Tech","base_url":"https://vtechworks.lib.vt.edu/oai/request"},"display":{"title":"The immunotoxic effects of aldicarb","abstract":"In the current studies the effects of administration of 0.1 to 1000 ppb of aldicarb, a carbamate pesticide, on the immune system of C3H mice were investigated. It was observed that aldicarb caused significant immunomodulation of macrophage functions analyzed in a variety of different systems. Initially, it was found that aldicarb decreased the stimulatory functions of the macrophages as studied by decreased capacity to stimulate normal autoreactive TF cells in the SMLR. This decreased stimulatory activity of the macrophages was found not to be due decrease in the expression of class II MHC-antigens (la molecules) nor was it due to the generation of any suppressor macrophages acting to down-regulate the immune response. Further investigations revealed that the decreased stimulatory activity of the macrophages correlated with decreased IL-1 production/signal to the T cells by the macrophages. It was also evident that aldicarb did not affect the T cell functions directly. Thus, T cells from aldicarb-treated mice when studied in the SMLR and AlloMLR or when stimulated with ConA or anti-CD3 mAbs, in the presence of normal macrophages, demonstrated normal responses. In contrast, normal T cells exhibited decreased responsiveness in the presence of aldicarb-treated macrophages. The fact that aldicarb did not affect the T cell functions directly was also evident by the fact that aidicarb-treated T cells could respond normally to stimulation with PMA + Ca²⁺ ionophore, a response which is independent of accessory cells. The aldicarb-treated macrophages also exhibited decreased capacity to process and present the antigen, conalbumin, to the T helper cell clone D10.G4. When the mechanism of aldicarb induced defect was investigated, it was observed that aldicarb-treated macrophages produced decreased amounts of IL-1 which was also confirmed by complete reconstitution of the response following addition of exogenous IL-1. With this in mind, macrophage functions in a number of other systems were examined and demonstrated that aldicarb-treatment also suppressed the macrophage-mediated cytotoxicity of tumor cells, but failed to inhibit the NK cell-mediated cytotoxicity of tumor cells. Together, these studies suggest that aldicarb selectively affects the macrophage but not NK or T ceil functions directly. However, since macrophages play an important role as accessory cells in T cell-mediated responses, it is likely that aldicarb indirectly will also affect the T cell responses.","abstract_html":"In the current studies the effects of administration of 0.1 to 1000 ppb of aldicarb, a carbamate pesticide, on the immune system of C3H mice were investigated. It was observed that aldicarb caused significant immunomodulation of macrophage functions analyzed in a variety of different systems. Initially, it was found that aldicarb decreased the stimulatory functions of the macrophages as studied by decreased capacity to stimulate normal autoreactive TF cells in the SMLR. This decreased stimulatory activity of the macrophages was found not to be due decrease in the expression of class II MHC-antigens (la molecules) nor was it due to the generation of any suppressor macrophages acting to down-regulate the immune response. Further investigations revealed that the decreased stimulatory activity of the macrophages correlated with decreased IL-1 production/signal to the T cells by the macrophages. It was also evident that aldicarb did not affect the T cell functions directly. Thus, T cells from aldicarb-treated mice when studied in the SMLR and AlloMLR or when stimulated with ConA or anti-CD3 mAbs, in the presence of normal macrophages, demonstrated normal responses. In contrast, normal T cells exhibited decreased responsiveness in the presence of aldicarb-treated macrophages. The fact that aldicarb did not affect the T cell functions directly was also evident by the fact that aidicarb-treated T cells could respond normally to stimulation with PMA + Ca²⁺ ionophore, a response which is independent of accessory cells. The aldicarb-treated macrophages also exhibited decreased capacity to process and present the antigen, conalbumin, to the T helper cell clone D10.G4. When the mechanism of aldicarb induced defect was investigated, it was observed that aldicarb-treated macrophages produced decreased amounts of IL-1 which was also confirmed by complete reconstitution of the response following addition of exogenous IL-1. With this in mind, macrophage functions in a number of other systems were examined and demonstrated that aldicarb-treatment also suppressed the macrophage-mediated cytotoxicity of tumor cells, but failed to inhibit the NK cell-mediated cytotoxicity of tumor cells. Together, these studies suggest that aldicarb selectively affects the macrophage but not NK or T ceil functions directly. However, since macrophages play an important role as accessory cells in T cell-mediated responses, it is likely that aldicarb indirectly will also affect the T cell responses.","abstract_has_math":false,"creators":["Dean, Timothy Neal"],"institution":"Virginia Tech","degree_name":"Master of Science","degree_level":"masters","degree_discipline":"Biology","degree_department":"Biology","school":null,"contributors":[],"advisors":[],"committee_chairs":["Nagarkatti, Prakash S."],"committee_members":["Nagarkatti, Mitzi","Stout, Ernest R."],"year":1990,"date_issued":"1990-01-05","date_published":"1990-01-05","updated_at":"2026-07-24T05:56:09Z","subjects":[],"languages":["en"],"rights":["In Copyright"],"rights_urls":["http://rightsstatements.org/vocab/InC/1.0/"],"identifier_entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["etd-03142009-040641"],"render_values":[{"text":"etd-03142009-040641","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/10919/41612","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.committeechair","label":"Committee Chair","values":["Nagarkatti, Prakash S."]},{"key":"dc:contributor.committeemember","label":"Committee Member","values":["Nagarkatti, Mitzi","Stout, Ernest R."]},{"key":"dc:contributor.department","label":"Department","values":["Biology"]},{"key":"dc:creator","label":"Author","values":["Dean, Timothy Neal"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2014-03-14T21:31:41Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2014-03-14T21:31:41Z","2009-03-14"]},{"key":"dc:date.issued","label":"Date","values":["1990-01-05"]},{"key":"dc:publisher","label":"Institution","values":["Virginia Tech"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]},{"key":"dc:type.dcmitype","label":"Dc Type Dcmitype","values":["Text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["masters"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science"]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["Virginia Polytechnic Institute and State University"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]},{"key":"dc:rights","label":"Dc Rights","values":["In Copyright"]},{"key":"dc:rights.uri","label":"Rights URI","values":["http://rightsstatements.org/vocab/InC/1.0/"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["etd-03142009-040641"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10919/41612"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["In the current studies the effects of administration of 0.1 to 1000 ppb of aldicarb, a carbamate pesticide, on the immune system of C3H mice were investigated. It was observed that aldicarb caused significant immunomodulation of macrophage functions analyzed in a variety of different systems. Initially, it was found that aldicarb decreased the stimulatory functions of the macrophages as studied by decreased capacity to stimulate normal autoreactive TF cells in the SMLR. This decreased stimulatory activity of the macrophages was found not to be due decrease in the expression of class II MHC-antigens (la molecules) nor was it due to the generation of any suppressor macrophages acting to down-regulate the immune response. Further investigations revealed that the decreased stimulatory activity of the macrophages correlated with decreased IL-1 production/signal to the T cells by the macrophages. It was also evident that aldicarb did not affect the T cell functions directly. Thus, T cells from aldicarb-treated mice when studied in the SMLR and AlloMLR or when stimulated with ConA or anti-CD3 mAbs, in the presence of normal macrophages, demonstrated normal responses. In contrast, normal T cells exhibited decreased responsiveness in the presence of aldicarb-treated macrophages. The fact that aldicarb did not affect the T cell functions directly was also evident by the fact that aidicarb-treated T cells could respond normally to stimulation with PMA + Ca²⁺ ionophore, a response which is independent of accessory cells. The aldicarb-treated macrophages also exhibited decreased capacity to process and present the antigen, conalbumin, to the T helper cell clone D10.G4. When the mechanism of aldicarb induced defect was investigated, it was observed that aldicarb-treated macrophages produced decreased amounts of IL-1 which was also confirmed by complete reconstitution of the response following addition of exogenous IL-1. With this in mind, macrophage functions in a number of other systems were examined and demonstrated that aldicarb-treatment also suppressed the macrophage-mediated cytotoxicity of tumor cells, but failed to inhibit the NK cell-mediated cytotoxicity of tumor cells. Together, these studies suggest that aldicarb selectively affects the macrophage but not NK or T ceil functions directly. However, since macrophages play an important role as accessory cells in T cell-mediated responses, it is likely that aldicarb indirectly will also affect the T cell responses."]},{"key":"dc:description.degree","label":"Dc Description Degree","values":["Master of Science"]},{"key":"dc:format.medium","label":"Dc Format Medium","values":["BTD"]},{"key":"dc:format.mimetype","label":"Dc Format Mimetype","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["The immunotoxic effects of aldicarb"]}]}],"canonical_facts":{"dc:contributor.committeechair":["Nagarkatti, Prakash S."],"dc:contributor.committeemember":["Nagarkatti, Mitzi","Stout, Ernest R."],"dc:contributor.department":["Biology"],"dc:creator":["Dean, Timothy Neal"],"dc:date.accessioned":["2014-03-14T21:31:41Z"],"dc:date.available":["2014-03-14T21:31:41Z","2009-03-14"],"dc:date.issued":["1990-01-05"],"dc:description.abstract":["In the current studies the effects of administration of 0.1 to 1000 ppb of aldicarb, a carbamate pesticide, on the immune system of C3H mice were investigated. It was observed that aldicarb caused significant immunomodulation of macrophage functions analyzed in a variety of different systems. Initially, it was found that aldicarb decreased the stimulatory functions of the macrophages as studied by decreased capacity to stimulate normal autoreactive TF cells in the SMLR. This decreased stimulatory activity of the macrophages was found not to be due decrease in the expression of class II MHC-antigens (la molecules) nor was it due to the generation of any suppressor macrophages acting to down-regulate the immune response. Further investigations revealed that the decreased stimulatory activity of the macrophages correlated with decreased IL-1 production/signal to the T cells by the macrophages. It was also evident that aldicarb did not affect the T cell functions directly. Thus, T cells from aldicarb-treated mice when studied in the SMLR and AlloMLR or when stimulated with ConA or anti-CD3 mAbs, in the presence of normal macrophages, demonstrated normal responses. In contrast, normal T cells exhibited decreased responsiveness in the presence of aldicarb-treated macrophages. The fact that aldicarb did not affect the T cell functions directly was also evident by the fact that aidicarb-treated T cells could respond normally to stimulation with PMA + Ca²⁺ ionophore, a response which is independent of accessory cells. The aldicarb-treated macrophages also exhibited decreased capacity to process and present the antigen, conalbumin, to the T helper cell clone D10.G4. When the mechanism of aldicarb induced defect was investigated, it was observed that aldicarb-treated macrophages produced decreased amounts of IL-1 which was also confirmed by complete reconstitution of the response following addition of exogenous IL-1. With this in mind, macrophage functions in a number of other systems were examined and demonstrated that aldicarb-treatment also suppressed the macrophage-mediated cytotoxicity of tumor cells, but failed to inhibit the NK cell-mediated cytotoxicity of tumor cells. Together, these studies suggest that aldicarb selectively affects the macrophage but not NK or T ceil functions directly. However, since macrophages play an important role as accessory cells in T cell-mediated responses, it is likely that aldicarb indirectly will also affect the T cell responses."],"dc:description.degree":["Master of Science"],"dc:format.medium":["BTD"],"dc:format.mimetype":["application/pdf"],"dc:identifier.other":["etd-03142009-040641"],"dc:identifier.uri":["http://hdl.handle.net/10919/41612"],"dc:language.iso":["en"],"dc:publisher":["Virginia Tech"],"dc:rights":["In Copyright"],"dc:rights.uri":["http://rightsstatements.org/vocab/InC/1.0/"],"dc:title":["The immunotoxic effects of aldicarb"],"dc:type":["Thesis"],"dc:type.dcmitype":["Text"],"thesis:degree_discipline":["Biology"],"thesis:degree_level":["masters"],"thesis:degree_name":["Master of Science"],"thesis:institution_name":["Virginia Polytechnic Institute and State University"]},"updated_at":"2026-07-24T05:56:09Z"}