Matthias Hesse- Cornell Veterinary Medicine

Faculty

Matthias Hesse

Assistant Professor of Immunology

Cornell University College of Veterinary Medicine
C5141 Veterinary Medical Center
E-mail: mh325
Phone: 607-253-3389

PhD (Alexander v. Humboldt University, Germany)

Dr. Hesse has been an Assistant Professor in the Department of Microbiology and Immunolgy since 2002. He received a diploma in biochemistry from the Free University in Berlin, Germany in 1994. Then he joined the German Research Center for Rheumatic Diseases (DRFZ) in Berlin, Germany, where he received his Ph.D. from the Alexander v.Humboldt University, Berlin in 1997. Later he spent 5 years at the National Institutes of Health in Bethesda, MD. He investigates the development of chronic inflammation in a model of schistosomiasis.

Research Interests / Lab Members / Related Links / Selected References

Research Interests

Chronic inflammation causes morbidity and mortality of a large number of patients worldwide. These diseases are weakly curable and often lead to lifelong treatments of patients, thereby adding a major economic burden. The further investigation of mechanisms, which control immune responses, will improve our understanding of inflammatory diseases and has the most promising potential for more effective means of treatment.

Helminthic parasites cause long-lasting infectious diseases, often accompanied by chronic inflammation. Their complicated life cycle requires a carefully orchestrated interaction with their mammalian host. They have to avoid being destroyed by the host’s immune system, and they also have to keep their host alive for relatively long time periods. Therefore, these infections constitute important models to investigate immunoregulation under conditions of chronic infection and inflammation. In schistosomiasis, a major tropical disease resulting from persistent infection with trematodes, female worms lay up to several hundred eggs daily for several years, most of which leave the host body. Significant numbers of eggs get accidentally trapped and induce vigorous local inflammatory responses. Numerous studies in mice and humans have demonstrated the importance of the egg-induced host T helper cell cytokine response for survival and pathology in acute and chronic schistosomiasis. This cytokine response is carefully controlled. Failure to establish or maintain a balanced immune response against parasite eggs has severe consequences for the host.

We investigate the role of immunosuppressive regulatory T cells as a potential regulatory mechanism in schistosomiasis. Our data demonstrate that CD4+Foxp3+ naturally-occurring regulatory T cells (naTreg) prevent exacerbated Th-2 cytokine responses in our model. Recent data indicate that many naTregs change to an active/memory phenotype when the disease progresses to chronic inflammation. We speculate that these cells are particularly important to control and maintain a balanced response in chronic schistosomiasis. We also explore whether these activated naTregs are able to crossregulate unrelated inflammatory responses in infected hosts. These results could explain the negative correlation between helminthic infections and allergic diseases. We expect that the results of this research will improve our knowledge regarding the disease etiology of chronic schistosomiasis and help to develop new treatment strategies for a variety of chronic inflammatory diseases.

Lab Members

Related Links

Disease facts and current developments (http://www.who.int/topics/schistosomiasis/en/)

University of Cambridge Department of Pathology Schistosomiasis Research Group (http://www.path.cam.ac.uk/~schisto/home-page.html)

An overview of the disease and some biology of the parasite:
Ross, A. G., Bartley, P. B., Sleigh, A. C., Olds, G. R., Li, Y., Williams, G. M., McManus, D. P.(2002). "Schistosomiasis." N Engl J Med 346:1212-20.

Selected References

Hesse, M., Cheever, A., W., Jankovic, D., Wynn, T. A. (2000). "NOS-2 mediates the protective anti-inflammatory and antifibrotic effects of the Th1-inducing adjuvant, IL-12, in a Th2 model of granulomatous disease." Am J Pathol 157:945-955.

Hesse, M., Modolell, M., La Flamme, A. C., Schito, M., Fuentes, J. M., Cheever, A. W., Pearce, E. J., Wynn, T. A.(2001). "Differential regulation of nitric oxide synthase-2 and arginase-1 by type 1/type 2 cytokines in vivo: granulomatous pathology is shaped by the pattern of L-arginine metabolism." J Immunol 167:6533-44.

Hoffmann, K. F., McCarty, T. C., Segal, D. H., Chiaramonte,, M.Hesse, Davis, E. M., Cheever, A., W.Meltzer, P. S., Morse, H. C., 3rd, Wynn, T. A. (2001). "Disease fingerprinting with cDNA microarrays reveals distinct gene expression profiles in lethal type 1 and type 2 cytokine-mediated inflammatory reactions." Faseb J 15:2545-7.

Hesse, M., C. A. Piccirillo, Y. Belkaid, J. Prufer, M. Mentink-Kane, M. Leusink, A. W. Cheever, E. M. Shevach, and T. A. Wynn. (2004). The pathogenesis of schistosomiasis is controlled by cooperating IL-10-producing innate effector and regulatory T cells. J Immunol 172:3157-3166.

Kaviratne, M., M. Hesse, M. Leusink, A. W. Cheever, S. J. Davies, J. H. McKerrow, L. M. Wakefield, J. J. Letterio, and T. A. Wynn. (2004). IL-13 activates a mechanism of tissue fibrosis that is completely TGF-beta independent. J Immunol 173:4020-4029.

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Last Revised on November 22, 2005