{"id":{"repo_id":"vcu","oai_identifier":"oai:scholarscompass.vcu.edu:etd-2003"},"canonical_url":"https://search.dev.ndltd.org/etd/vcu/oai:scholarscompass.vcu.edu:etd-2003","repository":{"repo_id":"vcu","name":"Virginia Commonwealth University","base_url":"https://scholarscompass.vcu.edu/do/oai/"},"display":{"title":"Influence of Anti-CD44 on Murine B Cell Activation","abstract":"Lymphocyte activation and trafficking are indispensable to the immune system. CD44, an adhesion molecule, plays important roles in T cell activation, lymphocyte homing/trafficking, and tumor metastasis. Although the functions of CD44 have been shown in T cells and other leukocytes, little is known about its role in B cells. The effects of CD44 cross-linking on murine B cell activation via CD40L/IL-4 was explored using the anti-CD44 mAbs RK3G9 and IM7. Immobilized RK3G9 and IM7 could strongly inhibit B cell proliferation and Ig production, with IgE inhibition being prominent. Soluble anti-CD44 had no effect. The inhibitory effect of RK3G9 was not influenced by addition of anti-FCγRII, indicating no role for the inhibitory receptor. The effects of delayed addition of immobilized anti-CD44 mAbs were studied, and the results indicated no inhibition after 96 hrs of culture. B cells were also activated by either LPS or anti-IgM F(ab')2. While LPS-induced B cell activation was inhibited by immobilized anti-CD44 mAbs, anti-IgM activation was refractory. Interestingly, addition of both anti-IgM and CD40L or LPS resulted in some modulation of the inhibitory activity. Additionally, FACS and Elispot revealed that RK3G9-treated cells had reduced numbers of plasma cells. Taken together, these results suggest that CD44 cross-linking could control polyclonal B cell activation by CD40L, but allow sIgM/CD40L activation to continue.","abstract_html":"Lymphocyte activation and trafficking are indispensable to the immune system. CD44, an adhesion molecule, plays important roles in T cell activation, lymphocyte homing/trafficking, and tumor metastasis. Although the functions of CD44 have been shown in T cells and other leukocytes, little is known about its role in B cells. The effects of CD44 cross-linking on murine B cell activation via CD40L/IL-4 was explored using the anti-CD44 mAbs RK3G9 and IM7. Immobilized RK3G9 and IM7 could strongly inhibit B cell proliferation and Ig production, with IgE inhibition being prominent. Soluble anti-CD44 had no effect. The inhibitory effect of RK3G9 was not influenced by addition of anti-FCγRII, indicating no role for the inhibitory receptor. The effects of delayed addition of immobilized anti-CD44 mAbs were studied, and the results indicated no inhibition after 96 hrs of culture. B cells were also activated by either LPS or anti-IgM F(ab')2. While LPS-induced B cell activation was inhibited by immobilized anti-CD44 mAbs, anti-IgM activation was refractory. Interestingly, addition of both anti-IgM and CD40L or LPS resulted in some modulation of the inhibitory activity. Additionally, FACS and Elispot revealed that RK3G9-treated cells had reduced numbers of plasma cells. Taken together, these results suggest that CD44 cross-linking could control polyclonal B cell activation by CD40L, but allow sIgM/CD40L activation to continue.","abstract_has_math":false,"creators":["Wyant, Tiana L."],"institution":null,"degree_name":"Doctor of Philosophy","degree_level":"Dissertation","degree_discipline":"Microbiology & Immunology","degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2006,"date_issued":"2006-01-01T08:00:00Z","date_published":"2006-01-01T08:00:00Z","updated_at":"2026-07-24T05:54:40Z","subjects":["CD44","lymphocyte activation","B cell","differentiation","Medicine and Health Sciences"],"languages":[],"rights":["© The Author"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarscompass.vcu.edu/etd/1004"],"render_values":[{"text":"https://scholarscompass.vcu.edu/etd/1004","href":"https://scholarscompass.vcu.edu/etd/1004","code":true}]}]},"links":{"outbound_url":"https://doi.org/10.25772/QZE1-BF44","outbound_label":"DOI","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Wyant, Tiana L."]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2014-07-09T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Microbiology & Immunology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Doctor of Philosophy"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["CD44","lymphocyte activation","B cell","differentiation","Medicine and Health Sciences"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["© The Author"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://doi.org/10.25772/QZE1-BF44","https://scholarscompass.vcu.edu/etd/1004"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Lymphocyte activation and trafficking are indispensable to the immune system. CD44, an adhesion molecule, plays important roles in T cell activation, lymphocyte homing/trafficking, and tumor metastasis. Although the functions of CD44 have been shown in T cells and other leukocytes, little is known about its role in B cells. The effects of CD44 cross-linking on murine B cell activation via CD40L/IL-4 was explored using the anti-CD44 mAbs RK3G9 and IM7. Immobilized RK3G9 and IM7 could strongly inhibit B cell proliferation and Ig production, with IgE inhibition being prominent. Soluble anti-CD44 had no effect. The inhibitory effect of RK3G9 was not influenced by addition of anti-FCγRII, indicating no role for the inhibitory receptor. The effects of delayed addition of immobilized anti-CD44 mAbs were studied, and the results indicated no inhibition after 96 hrs of culture. B cells were also activated by either LPS or anti-IgM F(ab')2. While LPS-induced B cell activation was inhibited by immobilized anti-CD44 mAbs, anti-IgM activation was refractory. Interestingly, addition of both anti-IgM and CD40L or LPS resulted in some modulation of the inhibitory activity. Additionally, FACS and Elispot revealed that RK3G9-treated cells had reduced numbers of plasma cells. Taken together, these results suggest that CD44 cross-linking could control polyclonal B cell activation by CD40L, but allow sIgM/CD40L activation to continue."]},{"key":"dc:title","label":"Title","values":["Influence of Anti-CD44 on Murine B Cell Activation"]}]}],"canonical_facts":{"dc:creator":["Wyant, Tiana L."],"dc:date.available":["2014-07-09T07:00:00Z"],"dc:description.abstract":["Lymphocyte activation and trafficking are indispensable to the immune system. CD44, an adhesion molecule, plays important roles in T cell activation, lymphocyte homing/trafficking, and tumor metastasis. Although the functions of CD44 have been shown in T cells and other leukocytes, little is known about its role in B cells. The effects of CD44 cross-linking on murine B cell activation via CD40L/IL-4 was explored using the anti-CD44 mAbs RK3G9 and IM7. Immobilized RK3G9 and IM7 could strongly inhibit B cell proliferation and Ig production, with IgE inhibition being prominent. Soluble anti-CD44 had no effect. The inhibitory effect of RK3G9 was not influenced by addition of anti-FCγRII, indicating no role for the inhibitory receptor. The effects of delayed addition of immobilized anti-CD44 mAbs were studied, and the results indicated no inhibition after 96 hrs of culture. B cells were also activated by either LPS or anti-IgM F(ab')2. While LPS-induced B cell activation was inhibited by immobilized anti-CD44 mAbs, anti-IgM activation was refractory. Interestingly, addition of both anti-IgM and CD40L or LPS resulted in some modulation of the inhibitory activity. Additionally, FACS and Elispot revealed that RK3G9-treated cells had reduced numbers of plasma cells. Taken together, these results suggest that CD44 cross-linking could control polyclonal B cell activation by CD40L, but allow sIgM/CD40L activation to continue."],"dc:identifier":["https://doi.org/10.25772/QZE1-BF44","https://scholarscompass.vcu.edu/etd/1004"],"dc:rights":["© The Author"],"dc:subject":["CD44","lymphocyte activation","B cell","differentiation","Medicine and Health Sciences"],"dc:title":["Influence of Anti-CD44 on Murine B Cell Activation"],"thesis:degree_discipline":["Microbiology & Immunology"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Doctor of Philosophy"]},"updated_at":"2026-07-24T05:54:40Z"}