Lab phone: 413-577-3316
Email: janguita [at] vasci [dot] umass [dot] edu
661 N Pleasant St
Amherst, MA 01003
Ph.D.: University of Leon, Spain, 1993
Postdoctoral Training: Yale University School of Medicine
Proinflammatory signals in response to infection
Proinflammatory signals in response to infection. Lyme disease is a highly prevalent infection in the United States. The disease is caused by the spirochete, Borrelia burgdorferi, which is transmitted by tick vectors, Ixodes scapularis and I. pacificus. Without proper treatment, the disease can evolve into inflammatory complications that most commonly affect the musculoskeletal, cardiovascular and nervous systems. Our lab is using the murine model of Lyme borreliosis to understand the role of signaling pathways such as NF-kB and MAP kinases in the development of proinflammatory responses in the context of infection. We are interested in the primary response to infectious agents triggered by their interaction with pattern recognition molecules, the effect of those interactions on the activation of iNKT and CD4 T cells, as well as the feedback mechanisms between both arms of the immune system. Part of our recent efforts are aimed at the understanding of the phagocytic uptake of the spirochete by macrophages.
Immunosuppression mediated by Salp15
Salp15 is a recently characterized antigen in tick saliva that has the capacity to inhibit the activation of naive CD4 T cells by repressing the calcium signals that arise upon TCR engagement. The final result is the inhibition of IL-2 production. Salp15 binds to the CD4 co-receptor on T cells and prevents early signals during activation. Our lab is currently analyzing the specificity of its function in murine as well as human T cells, and the potential application of this immunosuppressor in therapeutic intervention in several conditions that involve CD4 T cells.