Our research focuses on the regulation of T-cell responses, and the signals that determine the choice between effector and regulatory cells and between lymphocyte activation and tolerance.
Other Research in Dr. Abbas's Lab:
IgE antibodies can promote dangerous allergic reactions, such as anaphylaxis, and as a result the production of IgE is tightly regulated. We are interested in the cellular and molecular mechanisms that regulate IgE production and function.
Other Research in Dr. Allen' s Lab:
The Anderson lab is engaged in studies of immune regulation of autoimmune disease/responses. Methods used include the use of transfer systems, genetic knockouts, and classical genetic mapping studies.
Other Research in Dr. Anderson' s Lab:
The lineage decisions of helper T cells are often a decisive factor in the outcome of an immune response. We study the mechanisms by which T cells decide whether and how to respond to antigen encounter, with an emphasis on the role of small regulatory RNA, including microRNA.
Other Research in Dr. Ansel's Lab:
The research in my laboratory concerns the fundamental events that regulate T-cell activation during immune responses to autoantigens in diabetes in other autoimmune diseases. Our efforts to modulate T cell activation have centered on understanding and altering the positive signals delivered by the antigen-specific T cell receptor and secondary, so-called co-stimulatory signals, or engaging the negative regulatory events such as CTLA-4, PD-1 and Notch that control T cell signal transduction. The studies focus on the yin/yang of the CD28/CTLA-4 pathways which are essential for a homeostatic T cell response. We have used soluble receptor antagonists, monoclonal antibodies and animals deficient in individual members of the CD28/CTLA-4/B7 pathways to define their individual roles in autoimmunity. In addition, we are interested in the negative regulation of immunity focused on the role of PD-1/PD-L1 pathways in the control of tissue specific tolerance. Lastly, we have a major interest in regulatory T cells (Treg) that control immune homeostasis. Using a variety of approaches including two-photon microscopy, genetic manipulation and antagonist therapies, we hope to develop new insights into Treg function and therapeutic application. Together, the insights gained from these studies will help in the development of a new generation of tolerogenic drugs that will "turn off" selected parts of the immune system, leaving the disease-fighting capabilities intact.
Other Research in Dr. Bluestone's Lab:
Basophils are the scarcest of all circulating leukocytes. Despite residence in the blood and relative scarcity, we have found that these cells regulate allergic immune responses by controlling the recruitment of end effector cells (eosinophils) into tissue. Current goals of the lab include understanding how basophils regulate this process and the intercellular networks required for the allergic immune response.
Other Research in Dr. Cheng's Lab:
The Cyster lab studies the mechanisms regulating lymphocyte entry to and exit from lymphoid tissues during the immune response, and the role of regulatory T cells in reventing autoantibody responses.
Other Research in Dr. Cyster's Lab:
Differentiation of helper T cells to discrete subsets of effector cells remains a major interest of study. We use genetically modified mice to examine the acquisition of cytokine competence and the elaboration of cytokine proteins using both flow cytometric and tissue immunohistochemical methods to elucidate temporal and geographic elements in the response.
Other Research in Dr. Locksley's Lab:
An alternate synapse can form between adjacent activating T lymphocytes. We are investigating the role of this synapse in modulating T cell differentiation and potentially the decision between immunity and tolerance.
Other Research in Dr. Krummel's Lab:
Our work on cellular lymphoid homeostasis has focused on the cytokine receptor IL-15Ra. By generating and characterizing IL-15Ra deficient mice, we uncovered essential roles for IL-15Ra in multiple lymphoid cell types (Lodolce et al., Immunity. 1998). We used these mice to define essential roles for IL-15Ra in supporting CD8+ memory T cells and NK cells (Becker et al., J Exp Med. 2002; Burkett et al., PNAS. 2003; Koka et al., J Exp Med. 2003). Surprisingly, we found that virtually all of the effects of IL-15Ra signals in supporting lymphocytes are non-cell autonomous (Lodolce, J Exp Med. 2001; Burkett et al., PNAS. 2003; Koka et al., J Exp Med. 2003). Moreover, we have shown that this non-cell autonomous mechanism is in fact a unique cell biological mechanism of “trans-presentation,” i.e., IL-15Ra on the surface of accessory cells presents IL-15 in trans to low affinity IL-15Rb and gc receptors on lymphocytes (Burkett et al., J Exp Med. 2004; Koka et al., JI [Cutting Edge]. 2004). Ongoing studies focus on the specific locations and cell types involved in trans-presentation, and on the varied immunological consequences of this unique cytokine biology upon lymphocyte function.
Other Research in Dr. Ma's Lab:
Diverse types of immune cells interact in tissues to mount appropriate responses. Too much or too little can both lead to tissue dysfunction and pathology. The Molofsky labs uses in vivo tracking and manipulation of immune cells and cytokines to study the regulation and cellular cross-talk between immune cells and the tissue. We are currently focused on the cytokine IL-33 and the coordinate effects on regulatory and type 2 immune rresponses.
Other Research in Dr. Molofsky's Lab:
TGFβ is a pleiotropic cytokine with potent regulatory activity. We have shown that this cytokine can impact the immune response in regulatory T cell-dependent and -independent mechanisms. We are currently addressing how this cytokine controls adaptive immunity independent of regulatory T cells, focusing on the interplay between TGFβ and the common gamma chain cytokines signaling in memory CD8 T cell development and function. We are also interested in understanding the cellular source of TGFβ under steady state and pathogen induced inflammation.
Other Research in Dr. Sanjabi's Lab: