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Professor, Department of Internal Medicine,
Section of Rheumatology
Immunology-Microbiology, Internal Medicine
GME, Graduate College, Rush Medical College
1735 W. Harrison Street
Cohn Building
7th Floor
Chicago, IL 60612

(312) 942-7847
(312) 942-2808
PhD, Immunology
Animal Diseases, Biological Phenomena Cell Phenomena and Immunity, Biological Sciences, Genetic Processes, Immune System Diseases, Musculoskeletal Diseases
Animal surgery/Modeling, Cytokine Assessment, ELISA Development, Flow Cytometry, PCR, Transgenic Animal Technology/Microinjection, Western Northern Southern Blotting

Research Interest
Major Academic Community Activities
   Editorial Boards
   Invited Lectures
Major Accomplishments of Former Trainees 

Alison Finnegan, PhD, is a professor of internal medicine-rheumatology and professor of immunology/microbiology. She received her doctoral degree from Tufts University School of Medicine, Boston, Mass. and completed her postdoctoral training at National Institutes of Health, Bethesda, Md.. She continued as a senior staff fellow at the National Institutes of Health for three years before moving to Rush University School of Medicine in 1987.

Finnegan has served on the advisory board for Arthritis Foundation, American Cancer Society and Leukemia Research Foundation. Her research interest is in the area of rheumatoid arthritis, an autoimmune disease that targets the synovial joints. Finnegan’s laboratory is working with a model of rheumatoid arthritis induced in mice. Her work is aimed at understanding the mechanism controlling the induction and progression of arthritis specifically addressing the requirements for lymphocytes in the development of disease.

She is also assessing the role of biological therapies in the treatment of arthritis. Finnegan’s research is funded by the National Institute of Arthritis and Musculoskeletal and Skin Disease (NIAMS). Her work has been published in many professional journals, including Arthritis & Rheumatism, Journal of Immunology, and Autoimmunity.

Research Interest

Finnegan’s work is focus on understating the mechanism of disease in rheumatoid arthritis. Specifically her laboratory is working on a murine model of rheumatoid arthritis, proteoglycan-induced arthritis (PGIA). She has been continuously funded for last ten years by National Institutes of Health to examine the role of B cells in PGIA. She has found that PG-specific B cells are critical for the initiation and progression arthritis by acting as antigen presenting cells (APCs) for T cell activation.

This interaction between T cell and B cells is dependent on the expression of CD80 and CD86 co-stimulator molecules. Expression of CD80 and CD86 on other APC is not sufficient to overcome the loss of CD80 and CD86 on B cells. Similar to human rheumatoid arthritis depletion of B cells with antibodies to CD20 inhibits arthritis. In addition to a reduction in autoantibodies, PG-specific T cells are suppressed in B cell depleted mice. Interestingly, depletion of B cell also leads to an increase in the number and function of Foxp3 T regulatory cells.

The focus of the next few years will be to understand how the interaction between B cells in T regulatory cells controls disease. A component of this research will be to assess the T regulatory phenotype and function in rheumatoid arthritis patients before and after B cell depletion therapy.

The second area of research involves PG-specific CD4+ T cell cytokine production. She recently completed a 10 year NIH P01 grant and renewed this area of research in a new National Institutes of Health R01 grant. She has found that the microenvironment controls the type of T lymphocytes that is responsible for the development of arthritis. This is important because the specific environment where T lymphocytes are first activity may be responsible for the fact that RA is a very heterogeneous disease both in terms of severity and treatment outcomes. Thus, understanding how the environment regulates immune response will lead to more specific intervention.


RUMC Investigators:

  1. Carla Scanzello, MD, PhD: Section of Rheumatology, RUMC. – Finnegan is Scanzello’s faculty mentor for her current K08 award from NIAMS. Finnegan is a collaborator on Scanzello’s studies of CD14 in synovial fluid, and its role in modulating toll-like receptors cellular response.
  2. Katalin Mikecz, MD, PhD, and Tibor T. Glant MD, PhD Director of Molecule Medicine, Dept of Orthopedic Surgery RUMC. - Mikecz and Glant have been long term collaborators. We jointly held a 10-year PO1 grant from NIH NIAMS and presently Glant is co-investigator on 2 of Finnegan’s NIH R01 grants.
  3. Joshua Jacobs, MD: Dept of Orthopedic Surgery RUMC. -Finnegan provides expertise in the area of osteoimmunology for Jacobs' work.
  4. Nadim Hallab, PhD: Dept of Orthopedic Surgery RUMC. - Finnegan assists Hallab in inflammasome signaling using both in vitro and in vivo techniques.
  5. Meenakahi Jolly, MD: Section of Rheumatology, RUMC. -Finnegan assists Jolly with assess Lupus patients for the present of serum light chains.

National and International Collaborations:

  1. Marcus Clark, MD, PhD: Section Head of Rheumatology, University of Chicago, Chicago, Ill. - Clark and Finnegan are long-time collaborators on the role of B cells in RA. Three of Finnegan’s graduate students have gone to Clark’s laboratory as post-doctoral fellows.
  2. Yoichiro Iwakurs, PhD: Center for Experimental Medicine, Institute of Medical Science University of Tokyo, Tokyo, Japan. - Finnegan has collaboratored with Iwakurs on the role of IL-1 and IL-17 in animal models of arthritis.
  3. Linda Bradley, PhD, Scientist Biogen Idec. - Finnegan and Bradley have collaborator looking at the role of TWEAK molecule in arthritis.
  4. Lieping Chen, Ph.D. Department of Dermatology and Oncology, John Hopkins University, Baltimore MD. - Chen has collaborated with Finnegan on the role of program death (PD)-ligand (L) 1 in the regulation of arthritis.

Major Academic Community Activities

Editorial Boards

American College of Rheumatology
Abstract Chair
American Association of Immunologists
Major Symposium Annual Meeting
Senior Editor
Cellular Immunology
Associate Editor
National Institutes of Health
Hypersensitivity, Autoimmunity and Immune-Mediated Diseases (HAI)


Ph.D. Thesis Committees-Departments of Immunology/Micrology and Biocehmistry (>20)
Institutional Animal Care and Use Committee
Conflict of Individual Interest in Research (COIIR) Committee

Invited Lectures

Northwestern University Dept of Immunology
“The Route of Antigen Exposure Affects the Differentiation of Th1 and Th17 cells”
Indiana University, Indianapolis, IN
“B cells in Rheumatoid Arthritis”
Northwestern University Rheumatology Grand Rounds
“B cells in Rheumatoid Arthritis”
University of California Irvine, CA
“B cells”
American Association of Immunologist Annual Meeting
“B cell in Autoimmune Arthritis”
Henry Kunkel Society, New York, NY
“IFN-γ Regulates the Requirement for IL-7 in Promoting Proteogylcan-Induced Arthritis”
Novartis, Basel Switzerland
“Fc Receptor in Rheumatoid Arthritis”
Northwestern Rheumatology Grand Rounds
“B cell Depletion in Rheumatoid Arthritis”
Mayo Clinical Rochester, MN
“T cells Involvement in Proteoglycan-Induced Arthritis”
American College of Rheumatology Annual Meeting Basic Science Symposia
“B cells in Experimental Disease: New Insights”
35th Congress of the German Society of Rheumatology
“B cell Depletion in Rheumatic Disease”
27th European Workshop for Rheumatology Research, Florence, Italy
“The role of B cell in Rheumatoid Arthritis”

Publications (selected from 89 peer-reviewed publications)

  1. Nair A, Kanda V, Bush-Josph C, Verma, N, Chubinskaya, S, Mikecz, K, Glant, TT, Malfait A-M, Crow MK, Spear T, Finnegan A, Scanzello CR. Synovial fluid from patients with early osteoarthritis modulates fibroblast-like synoviocyte responses to TLR-4 and TLR-2 ligands voa soluble CD14. Arthritis & Rheum, (in press 2012)
  2. Finnegan A., Ashaye S., Hamel KM. B effector cells in rheumatoid arthritis and experimental arthritis. Autoimmunity (in press 2012)
  3. Hamel KM, Cao Y, Ashaye S, Wang Y, Dunn R, Kehry MR, Glant TT, Finnegan A. B cell depletion enhances T regulatory cell activity essential in the suppression of arthritis. J Immunol. 2011 Nov 1;187(9):4900-6. Epub 2011 Sep 23. [PMID: 21948985]
  4. Aggarwal R, Sequeira W, Kokebie R, Mikolaitis RA, Fogg L, Finnegan A, Plaas A, Block JA, Jolly M. Serum free light chains as biomarkers for systemic lupus erythematosus disease activity. Arthritis Care Res (Hoboken). 2011 Jun;63(6):891-8. doi: 10.1002/acr.20446. [PMID: 21312346]
  5. Glant TT, Radacs M, Nagyeri G, Olasz K, Laszlo A, Boldizsar F, Hegyi A, Finnegan A, Mikecz K. Proteoglycan-induced arthritis and recombinant human proteoglycan aggrecan G1 domain-induced arthritis in BALB/c mice resembling two subtypes of rheumatoid arthritis. Arthritis Rheum. 2011 May;63(5):1312-21. doi:10.1002/art.30261. [PMID: 21305522]


1.  NIH-NIAMS R01 AR47657 “B cell Function in Autoimmune Arthritis”,
     Total award:  $1,583,600
     Grant Period  04/05/07-03/31/12
2.  NIH-NIAID R01 AR056999 “Cytokine Regulation in Experimental Arthritis”
     Total award:  $1,665,000
     Grant Period  04/0109-03/31/14

Major Accomplishments of Former Trainees

Finnegan has been teaching at Rush Medical College since 1990 and is currently the director of basic immunology. In her years at Rush, Finnegan has been doctorate thesis advisor to eleven graduate students and has mentored five post-doctoral/clinical fellows. Selected Major Accomlishments:

Keith Hamel, PhD 2011 University of Chicago

  1. Mandal M, Powers SE, Maienschein-Chine M, Bartom ET, Hamel KM, Kee BL, Dinner Clark MR. Epigenetic repression of the Igk locus by Stat-5 mediated recruitment of the histone methytransferase Ezh2. Nature Immunology, 12:1212, 2011.  

Shannon O’Neal, PhD 2005 National Jewish Health, Denver, CO

  1. O’Neill SK, Getahun A, Gauld SB, Merrell KT, Tamir I, smith MJ, Dal Porto JM, Li QZ, Cambier JC. Monophosphorylation of CD79a and CD79b ITAM motifs initiates a SHIP-1 phosphatase-mediated inhibitory signaling cascade required for B cell anergy. Immunity, 35:746, 2011.  

Charles Kaplan, PhD 2003 Senior Research Associate, Genetech San Francisco, CA

  1. Crellin NK, Trifari S, Kaplan CD, Cupedo T, Sits H. Human NKp44+IL-222+ cells and LTi-like cells constitute a stable RORC+ lineage distinct from conventional natural killer cells. Journal Experimental Medicine, 207:281, 2010.  

Karyn Siemasko, PhD 1996 Scientist Allergan, Irvine, CA

  1. Schaumburg CS, Siemasko KF, De Paiva CS, Wheeler LA, Niederkorn JY, Pflugfelder SC, Stern ME. Ocular surface APCs are necessary for autoreactive T cell-mediated experimental autoimmune lacrimal keratoconjunctivitis. Journal of Immunology, 187:3653, 2011.  
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