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Catherine Calkins, PhD

Contact Dr. Calkins

1020 Locust Street
Philadelphia, PA 19107

(215) 503-7950

Research and Clinical Interests

One project on-going in my laboratory is an investigation of the normal mechanisms of regulating immune responsiveness to self antigens.

Specifically, we are studying the response to self erythrocytes (MRBC) in normal BALB/c mice and in NZB mice that spontaneously develop anti-MRBC responses by 6-9 months of age. We have demonstrated that both T and B cells reactive to self erythrocytes are present in normal as well as autoimmune mice. In culture, development of anti-erythrocyte autoantibody responses depend upon CD4 positive helper T cells and can be suppressed by CD8 positive T cells. Studies in the literature have suggested that the NZB autoantibodies are specific for Band 3 on erythrocyte membranes. In collaboration with Dr. Peter Curtis (Department of Microbiology), we are investigating the specific epitope on the Band 3 molecule that is recognized by NZB autoantibodies and by the autoimmune B cells detectable in normal mice. We will also determine if there are any changes in the fine specificity of the anti-self erythrocyte response throughout the course of the autoimmune disease in the NZB mice.

The second project, being done in collaboration with Dr. Mark Feitelson (Dept. of Pathology), is an investigation of the immune responses that cause chronic hepatitis B. We are studying a mouse model of the disease in which immunodeficient SCID mice, expressing HBV as a transgene, are given immunocompetent lymphocytes as adults. After 3-12 weeks, these mice begin to show signs of hepatitis, including liver enzymes in the circulation, loss of HBV envelope expression in the liver, and cellular infiltrates into the liver. We are now analyzing the immune cells of these mice to determine the nature of the immune reactivity to HBV in terms of specificity and cytokine production, size of response and timing. We are also comparing the responses developed during chronic disease with those developed during acute disease in order to gain an understanding of the regulatory mechanisms contributing to development of disease.