The dual roles of interleukin-2 during T cell activation / by Marcus S. Norris, Jr.
| Author/creator | Norris, Marcus S. author. |
| Other author | Mannie, Mark D., degree supervisor. |
| Other author | Kalmus, Gerhard W., degree supervisor. |
| Other author | East Carolina University. Department of Biology. |
| Format | Theses and dissertations |
| Production | 2002. |
| Description | vii, 72 leaves : illustrations ; 28 cm |
| Supplemental Content | Access via ScholarShip |
| Subjects |
| Summary | The purpose of this thesis is to study the immunogenic versus tolerogenic activities of IL-2. The cytokine interleukin-2 (IL-2) has been long regarded as the primary T cell growth factor of the immune system. IL-2 is secreted by T cells upon antigenic activation. It binds nearby T cells, augmenting the activation of those cells and also serves in a positive feedback loop by promoting further IL-2 production from the T cell. Paradoxically, IL-2 deficient mice demonstrate an immunoproliferative disorder that occurs spontaneously and is characterized by T cell dependent inflammation against selfantigens and normally non-pathogenic intestinal flora. These previous studies suggest dual functions of IL-2 in that this cytokine is not only required for cell survival and activation in vitro, but also has inhibitory activity required for peripheral tolerance in vivo. Specifically, this study shows that IL-2 promotes antigenic responsiveness, subsequent reactivity to antigen, and increases cell surface activation markers and adhesion molecules on rested T cells. IL-2 may thereby prime na̐ve or non-activated T cells. The data also indicates that IL-2 may have an inhibitory role in T cell activation. After activation, T cells undergo a refractory phase in which T cells have decreased responsiveness to additional antigen exposure. This refractory phase may last up to 14 days following activation. Hence, "rested" T cells (i.e., those cells that have not been recently activated by antigen) are much more responsive to antigen than recently activated T cells. The data in this study shows that IL-2 was able to prolong the refractory phase, inhibit cell cycle proliferation and decrease the IL-2-induced proliferation of activated T cells. These findings suggest IL-2 may have alternate functions depending upon the activation state of the T cell. |
| General note | Presented to the faculty of the Department of Biology. |
| General note | Advisor: Mark D. Mannie |
| General note | Advisor: Gerhard Kalmus |
| Dissertation note | M.S. East Carolina University 2002 |
| Bibliography note | Includes bibliographical references (leaves 64-72). |
| Genre/form | dissertations. |
| Genre/form | Academic theses. |
| Genre/form | Academic theses. |
| Genre/form | Thèses et écrits académiques. |
Availability
| Library | Location | Call Number | Status | Item Actions |
|---|---|---|---|---|
| Joyner | University Archives | ASK AT SPECIAL COLLECTIONS DESK | ✔ Available | Request Material |
| Electronic Resources | ✔ Available |