Department of Pathology, Microbiology, and Immunology



Kyra Richter, Ph.D.



Research Assistant Professor

Dept. of Pathology, Microbiology and Immunology



Contact Information



Office Location:
MCN A-3314

Phone: 615-322-5266
E-mail:  kyra.richter@vanderbilt.edu


Campus Mail:

Pathology, Microbiology and Immunology-5th Fl

MCN A-5301 (2363)


Mailing address:
Vanderbilt University School of Medicine

Department of Pathology, Microbiology and Immunology-5th Fl
MCN A-5301
1161 21st Ave. S.

Nashville, TN 37232-2363



Research Keywords



human immunology, T lymphocytes, infectious disease, sarcoidosis, granulomatous inflammation



Research Description



The focus of my research is to study the role of the adaptive immune system in disease pathogenesis and to clearly define the mechanisms that regulate pathogenesis. By dissecting the host-cell interactions in granulomatous inflammation, I hope to identify host factors that may be exploited for novel therapies in chronic lung disease. Moreover, by investigating the role of individual cell subsets in granulomatous formation and maintenance, I hope to gain insight into how granulomatous inflammation is initiated and progresses to chronicity.
Currently, I use sarcoidosis as a model system for granulomatous inflammation. Sarcoidosis is a unique disease which is at the crossroads of microbial infection and host immune response. Specifically, sarcoidosis is a multisystem granulomatous disease of unknown etiology, characterized by a T helper 1 (Th1) immunophenotype. Although sarcoidosis is a systemic disease, it most commonly affects the lungs. The immune response in sarcoidosis has been well characterized, however the lack of antigen has hindered in-depth analyses of the role of specific cells in sarcoidosis pathogenesis. Recent reports from independent laboratories have postulated mycobacteria as a candidate. The potential role of mycobacteria in sarcoidosis immunopathogenesis has been demonstrated by the detection of mycobacterial proteins and nucleic acids in sarcoidosis granulomas, as well as humoral and peripheral cellular immune responses to mycobacterial antigens in sarcoidosis subjects. In addition, our lab has made significant advances in studying the immune response to mycobacterial antigens at the site of active sarcoidosis involvement a?? the lungs. Our lab has demonstrated the presence of antigen-specific recognition of mycobacterial proteins in CD4+ and CD8+ T cells derived from sarcoidosis subjects at diagnostic bronchoscopy. The current focus is to delineate CD8+ molecular and biologic T cell function in sarcoidosis pathogenesis and how it influences sarcoidosis resolution or progression. In addition, we are interested in how HLA types correlate with disease outcome.






Oswald-Richter, K, Sato, H, Hajizadeh, R, Shepherd, BE, Sidney, J, Sette, A, Newman, LS, Drake, WP. Mycobacterial ESAT-6 and katG are Recognized by Sarcoidosis CD4+ T Cells When Presented by the American Sarcoidosis Susceptibility Allele, DRB1*1101. J Clin Immunol, 30(1), 157-66, 2010

Oswald-Richter, KA, Culver, DA, Hawkins, C, Hajizadeh, R, Abraham, S, Shepherd, BE, Jenkins, CA, Judson, MA, Drake, WP. Cellular responses to mycobacterial antigens are present in bronchoalveolar lavage fluid used in the diagnosis of sarcoidosis. Infect Immun, 77(9), 3740-8, 2009

Antons, AK, Wang, R, Oswald-Richter, K, Tseng, M, Arendt, CW, Kalams, SA, Unutmaz, D. Naive precursors of human regulatory T cells require FoxP3 for suppression and are susceptible to HIV infection. J Immunol, 180(2), 764-73, 2008

Oswald-Richter, K, Grill, SM, Leelawong, M, Tseng, M, Kalams, SA, Hulgan, T, Haas, DW, Unutmaz, D. Identification of a CCR5-expressing T cell subset that is resistant to R5-tropic HIV infection. PLoS Pathog, 3(4), e58, 2007

Carlisle, J, Evans, W, Hajizadeh, R, Nadaf, M, Shepherd, B, Ott, RD, Richter, K, Drake, W. Multiple Mycobacterium antigens induce interferon-gamma production from sarcoidosis peripheral blood mononuclear cells. Clin Exp Immunol, 150(3), 460-8, 2007

Dillon, S, Agrawal, S, Banerjee, K, Letterio, J, Denning, TL, Oswald-Richter, K, Kasprowicz, DJ, Kellar, K, Pare, J, van Dyke, T, Ziegler, S, Unutmaz, D, Pulendran, B. Yeast zymosan, a stimulus for TLR2 and dectin-1, induces regulatory antigen-presenting cells and immunological tolerance. J Clin Invest, 116(4), 916-28, 2006

Oswald-Richter, K, Torres, VJ, Sundrud, MS, VanCompernolle, SE, Cover, TL, Unutmaz, D. Helicobacter pylori VacA toxin inhibits human immunodeficiency virus infection of primary human T cells. J Virol, 80(23), 11767-75, 2006

VanCompernolle, SE, Taylor, RJ, Oswald-Richter, K, Jiang, J, Youree, BE, Bowie, JH, Tyler, MJ, Conlon, JM, Wade, D, Aiken, C, Dermody, TS, KewalRamani, VN, Rollins-Smith, LA, Unutmaz, D. Antimicrobial peptides from amphibian skin potently inhibit human immunodeficiency virus infection and transfer of virus from dendritic cells to T cells. J Virol, 79(18), 11598-606, 2005

Oswald-Richter, K, Grill, SM, Shariat, N, Leelawong, M, Sundrud, MS, Haas, DW, Unutmaz, D. HIV infection of naturally occurring and genetically reprogrammed human regulatory T-cells. PLoS Biol, 2(7), E198, 2004

Oswald-Richter, K, Grill, SM, Leelawong, M, Unutmaz, D. HIV infection of primary human T cells is determined by tunable thresholds of T cell activation. Eur J Immunol, 34(6), 1705-14, 2004