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WILDER, JULIE A., PHD CONTACT INFORMATION Fax: (505) 348-8567 e-mail: jwilder@LRRI.org Extended CV

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EDUCATION
B.A. (Biology) 1983, Grinnell College
Ph.D. (Microbiology) 1990, University of Iowa

EMPLOYMENT

2002 - Present	Associate Scientist, Respiratory Immunology and Asthma Program, Lovelace Respiratory Research Institute, Albuquerque, NM
2002 - Present	Adjunct Assistant Professor, Department of Pathology, University of New Mexico, Albuquerque, NM
1996 - 2001	Research Assistant Professor, Department of Pathology, University of New Mexico, Albuquerque, NM
1994 - 1996	Postdoctoral Fellow, Department of Pathology, University of New Mexico, Albuquerque, NM
1990 - 1994	Postdoctoral Fellow, Department of Pathology, University of Texas Southwest Medical Center, Dallas, TX
1984 - 1988	Teaching Assistant, Department of Microbiology, University of Iowa, Iowa City, IA

HONORS
NIH Immunology Training Grant CA09082, 3/90-2/91
Pulmonary Epidemiology and Toxicology Training Program Fellow (Jointly
     administered by the University of New Mexico School of Medicine and the
     Inhalation Toxicology Research Institute), 2/95-1/97
American Association of Immunologists Faculty Mentor/Minority Trainee
     Travel Awards to attend the 2004 and 2005 Experimental Biology Meeting



AREAS OF RESEARCH
The human lung is exposed daily to 10,000 L of inspired air containing non-infectious particulate and soluble matter, and microbes. Occasionally, an immune response is mounted to combat the invasion of infectious microorganisms, and most often, this immune response serves to clear the offending organism from the host. In rare cases, an ineffective immune response can result in chronic infection and inflammation in the lung. Some individuals, due in part to their genetic background, mount an aberrant immune response to a non-infectious particle, referred to as an allergen, which can also result in chronic inflammation in the lung. Chronic inflammation induced by either an ineffective or aberrant immune response can damage the lung irreversibly resulting in high morbidity and even mortality. Our laboratory is interested in understanding the development and consequences of immune responses that manifest themselves in the lung. We use two murine models of disease to study pulmonary immunity. One model involves infection of mice with the pulmonary fungal pathogen Cryptococcus neoformans, whereas the other is a model of allergic asthma. We are particularly interested in understanding which genes are expressed during both Type 1 (characterized by IFNg production) and Type 2 (typified by IL-4, IL-5 and IL-13 secretion) pulmonary immune responses. We are currently undertaking a quantitative trait loci analysis of Cryptococcus infected mice and analyzing pulmonary gene expression in such mice using microarray technology. We are also currently investigating how environmental tobacco smoke exposure contributes to the development and chronicity of the allergic asthmatic response in the lung.

REPRESENTATIVE PUBLICATIONS

1. Yuan, D., C. Koh and J. A. Wilder: Interactions Between B Lymphocytes and NK Cells. FASEB J. 8: 1012-1018, 1994.

2. Wilder, J. A. and D. Yuan: Regulation of IFN-gamma mRNA Production in Murine Natural Killer Cells. Int. Immunol. 7: 575-582, 1995.

3. Wilder, J. A., C. Y. Koh and D. Yuan: The Role of NK Cells During In Vivo Antigen-Specific Antibody Responses. J. Immunol. 156: 146-152, 1996.

4. Schuyler, M. and J. A. Wilder: T Lymphocyte Subpopulations in Human Allergic Disease. In T Lymphocyte Subpopulations in Immunotoxicology (M. J. Selgrade and I. Kimber, eds.), pp. 233-252, Zeneca, 1998.

5. Cheung, J. C., C. Y. Koh, B. E. Gordon, J. A. Wilder and D. Yuan: The Mechanism of Activation of NK-Cell IFNg Production by Ligation of CD28. Mol. Immunol. 36: 361-372, 1999.

6. Lipscomb, M. F., C. R. Lyons, A. A. Izzo, J. A. Lovchik and J. A. Wilder: Experimental Pulmonary Cryptococcus Infection in Mice. In Handbook of Animal Models of Infection (O. Zak and M. A. Sande, eds.), Academic Press Ltd., 1999.

7. Lipscomb, M. F. and J. A. Wilder: Immune Dysregulation as a Cause for Allergic Asthma. Curr. Opin. Pulm. Med. 5: 10-20, 1999.

8. Lovchik, J. A., J. A. Wilder, G. B. Huffnagle, R. Riblet, C. R. Lyons and M. F. Lipscomb: Ig Heavy Chain Complex-Linked Genes Influence the Immune Response in a Murine Cryptococcal Infection. J. Immunol. 163: 3907-3913, 1999.

9. Wilder, J. A., D. D. S. Collie, B. S. Wilson, D. E. Bice, C. R. Lyons and M. F. Lipscomb: Dissociation of Airway Hyperresponsiveness from Immunoglobulin E and Airway Eosinophilia in a Murine Model of Allergic Asthma. Am. J. Respir. Cell. Mol. Biol. 20: 1326-1334, 1999.

10. Lipscomb, M. F., A. Izzo, J. A. Wilder, J. A. Lovchik and C. R. Lyons: Factors Regulating Effective T-Cell Immunity in the Lung. Eur. Respir. Rev. 10: 70, 103-107, 2000.

11. Wilder, J. A., D. D. Collie, D. E. Bice, Y. Tesfaigzi, C. R. Lyons and M. F. Lipscomb: Ovalbumin Aerosols Induce Airway Hyperreactivity in Naïve DO11.10 T Cell Receptor Transgenic Mice Without Pulmonary Eosinophilia or OVA-Specific Antibody. J. Leukoc. Biol. 69: 538-547, 2001.

12. Barrett, E. G., J. A. Wilder, T. H. March, T. Espindola and D. E. Bice: Cigarette Smoke-Induced Airway Hyperresponsiveness is not Dependent on Elevated Immunoglobulin and Eosinophilic Inflammation in a Mouse Model of Allergic Airway Disease. Am. J. Respir. Crit. Care Med. 165: 1410-1418, 2002.

13. Tesfaigzi, Y., M. J. Fischer, M. Daheshia, F. H. Y. Green, G. T. De Sanctis and J. A. Wilder: Bax is Crucial for IFN-g-Induced Resolution of Allergen-Induced Mucous Cell Metaplasia. J. Immunol. 169: 5919-5925, 2002.

14. Wilder, J. A., G. K. Olson, Y. C. Chang, K. J. Kwon-Chung and M. F. Lipscomb: Complementation of a Capsule Deficient Cryptococcus neoformans with CAP64 Restores Virulence in a Murine Lung Infection. Am. J. Respir. Cell. Mol Biol. 26: 306-314, 2002.

15. Hernandez-Hansen, V., J. D. Bard, C. A. Tarleton, J. A. Wilder, C. A. Lowell, B. S. Wilson and J. M. Oliver: Increased Expression of Genes Linked to FceRI Signaling and to Cytokine and Chemokine Production in Lyn-Deficient Mast Cells. J. Immunol. 175(12): 7880-7888, 2005.

16. Gao, N., P. Schwartzberg, J. A. Wilder, B. R. Blazar and D. Yuan: B Cell Induction of IL-13 Expression in NK Cells: Role of CD244 and SLAM-Associated Protein. J. Immunol. 176(5): 2758-2764, 2006.

17. March, T. H., J. A. Wilder, D. C. Esparza, P. Y. Cossey, L. F. Blair, L. K. Herrera, J. D. McDonald, M. J. Campen, J. L. Mauderly and J. Seagrave: Modulators of Cigarette Smoke-Induced Pulmonary Emphysema in A/J Mice. Toxicol. Sci. 92(2): 545-559, 2006.

18. Pierce, J., J. Rir-Sima-ah, I. Estrada, J. Wilder, A. Strasser and Y. Tesfaigzi: Loss of Pro-apoptotic Bim Promotes Accumulation of Pulmonary T Lymphocytes and Enhances Allergen-Induced Goblet Cell Metaplasia. Am. J. Physiol. Lung Cell. Mol. Physiol. 291(5): L862-L870, 2006.

19. Lipscomb, M. F., J. A. Wilder and B. J. Masten: Chapter 2, Dendritic Cells and Their Role in Linking Innate and Adaptive Immune Responses. In The Biology of Dendritic Cells and HIV Infection (S. Gessani and F. Belardelli, eds.), pp. 45-84, Springer, 2007.

20. Scott, B. R., S. A. Belinsky, S. Leng, Y. Lin, J. A. Wilder and L. A. Damiani: Radiation-Stimulated Epigenetic Reprogramming of Adaptive-Response Genes in the Lung: An Evolutionary Gift for Mounting Adaptive Protection Against Lung Cancer. Dose-Response 7(2): 104-131, 2009.