Brooks, Kathryn H.

Kathryn H. Brooks

Professor Emeritus

B.A., 1969, Washington University
Ph.D., 1981, University of Iowa
Postdoctoral Fellow, 1981-1986, University of Texas Health Science Center at Dallas


The research in my laboratory is focused on the ability of neoplastic B cells to alter responses of non-transformed B cells. Normally, tumor-host interactions are viewed from the perspective of the immune system's capacity to react with and eliminate the tumor. However, the immune system is a highly interactive system. When one portion of this system alters its function due to transformation, the change can impact the function of other cells within the system.

Our current studies involve the characterization of B cell activation events initiated by cell-cell contact with a CD5+ neoplastic B cell population. These cell-cell interactions between normal and transformed B cells induces a capacity to respond to interleukin 2 (IL-2) in the normal B cell population. In addition to the contact-mediated signal, the neoplastic B cell provides cytokines (IL-10 and possibly IL-6) which enhance the proliferative response to exogeneous IL-2. Our primary objectives are a) to identify the surface molecules which mediate the contact-dependent signal, b) elucidate the intracellular activation events triggered by the contact-dependent signal, and c) determine the mechanisms by which the neoplastic B cell-derived cytokines enhance proliferation. Completion of these objectives will provide the information necessary to evaluate the physiological significance of these interactions using in vivo models.

To date, most of our work has been done in a murine experimental model. Some preliminary studies have demonstrated a similar form of B cell activation using human cell lines and peripheral blood lymphocytes. Future studies will focus on developing an in vitro model system for post-transplant lymphoproliferative disorder (PTLD). PTLD occurs in up to 10% of transplant patients and involves the outgrowth of Epstein-Barr virus (EBV) transformed B cells. In normal individuals, EBV transformed B cells are eliminated by immune surveillance mechanisms. However, in transplant patients, the immunosuppressive therapy required to ensure long-term survival of the graft allows the emergence of an EBV+ B cell population. These EBV transformed B cells are known to secrete significant quantities of both IL-10 and IL-6. Thus, if they also possess the surface molecules required for the contact-dependent signal observed in the murine system, proliferation of the normal B cell population may be occurring whenever sufficient IL-2 is present. The development of an in vitro model using in vitro EBV transformed B cells and syngeneic peripheral blood B cells will allow us to address this possibility.