Susan A. Boackle
M.D.
Associate Professor of Medicine

Education: 

B.S., Molecular Biology, Vanderbilt University, Nashville, Tennessee

M.D., University of Alabama School of Medicine, Birmingham, Alabama

Postgraduate training:

When arrived at UCD:  1996

Past and current professional positions:

Board certification: Internal Medicine, Rheumatology

Community service:

Board of Directors, Arthritis Foundation, Rocky Mountain Chapter

Health Advisory Committee, Lupus Foundation of Colorado

National service:

Medical/Scientific Advisory Council, Lupus Foundation of America

Councillor, Western Section Council, American Federation of Medical Research

Awards and Honors received:

Harmon Arthritis Research Award, Arthritis Foundation, Rocky Mountain Chapter, 2002

AAI Junior Faculty Travel Award, 2002

Lupus Foundation of Colorado Research Grant, 2007

Description of research interests and/or clinical trial interests:

My laboratory is interested in the pathogenesis of autoimmune disease, focusing on genes involved in the development of SLE. Using a mouse model for lupus, we have identified the Cr2 gene, which encodes complement receptor type 2 (CR2), to be a strong candidate gene for lupus susceptibility. In addition, my laboratory has recently shown that the ubiquitously expressed complement regulatory gene, Crry, has structural and functional alterations that may predispose to development of SLE.  Ongoing studies are being performed to prove the role of these genes in this mouse model of lupus and to understand the mechanisms by which they contribute to disease pathogenesis.

In collaboration with Dr. Betty Tsao at UCLA and Dr. Daniela Ulgiati at the University of Western Australia, we have now shown that the CR2 gene is also associated with human lupus.  Continuing collaborative studies are underway to identify the causative polymorphisms for this association and to characterize the mechanisms by which they confer susceptibility to lupus, in order to identify therapeutic options that can be tested in individuals with SLE. 

Finally, my laboratory is investigating whether CR2 levels, which have been shown to be low in SLE, are a biomarker for lupus disease activity.  We are evaluating adults and children with lupus serially over time to determine whether monitoring CR2 levels will enable us to better manage and treat their lupus.

Representative publications:

1. Boackle, S.A., Holers, V.M., Karp, D.R. 1997. CD21augments antigen presentation in immune individuals. Eur J Immunol 27: 122-130.

2. Boackle, S.A., Morris, M.A., Holers, V.M., Karp, D.R. 1998. Complement opsonization is required for presentation of immune complexes by resting peripheral blood B cells. J Immunol 161: 6537-6543. 


3. Henson, S.E., Smith, D., Boackle, S.A., Holers, V.M., Karp, D.R. 2001. Generation of recombinant human C3dg tetramers for the analysis of CD21 binding and function. J Immunol Methods 258: 97-109.

4. Boackle, S.A., Holers, V.M., Chen, X., Szakonyi, G., Karp, D.R., Wakeland, E.K., Morel, L. 2001. Cr2, a candidate gene in the murine Sle1c lupus susceptibility locus, encodes a dysfunctional protein. Immunity 15: 775-785.

5. Boackle, S.A., Culhane, K.K., Brown, J.B., Haas, M., Bao, L., Quigg, R.J., and Holers, V.M. 2004. CR1/CR2 deficiency alters IgG3 autoantibody production and IgA glomerular deposition in the MRL/lpr model of SLE. Autoimmunity 37: 111-123.

6. Chen, Y., Perry, D., Boackle, S.A., Sobel, E.S., Molina, H., Croker, B.P., and Laurence Morel. 2005. Several genes contribute to the production of autoreactive B and T cells in the murine lupus susceptibility locus Sle1c. J Immunol 175: 1080-1089.

7. Wu, H.*, Boackle, S.A.*, Hanvivadhanakul, P.*, Ulgiati, D.*, Grossman, J.M., Lee, Y., Shen, N., Abraham, L.J., Mercer, T.R., Park, E., Hebert, L.A., Rovin, B.H., Birmingham, D.J., Chang, D.-M., Chen, C.J., McCurdy, D., Badsha, H.M., Thong, B.Y.H., Chng, H.H., Arnett, F.C., Wallace, D.J., Yu, C.Y., Hahn, B.H., Cantor, R.M., Tsao, B.P. 2007. Association of a common complement receptor 2 haplotype with increased risk of systemic lupus erythematosus. Proc Natl Acad Sci 104: 3961-3966. (*These authors contributed equally to this work.)

8. Giles, B.M., Tchepeleva, S.N, Kachinski, J.J., Ruff, K., Croker, B.P., Morel, L., and Boackle, S.A. 2007. Augmentation of NZB autoimmune phenotypes by the NZW-derived Sle1c lupus susceptibility interval. J Immunol 178: 4667-4675.

9. Tchepeleva, S.N., Thurman, J.M., Perkins, S., Morel, L., and Boackle, S.A. 2007. Enhanced complement regulatory function of an allelic variant of Crry in the murine Sle1c lupus susceptibility interval. (submitted)