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Christina Hirsch, M.D., Ph.D.

Associate Professor of Medicine, Case Western Reserve University

Division of Infectious Diseases & HIV Medicine

Email : christina.hirsch@uhhospitals.org
Office Phone : 216.844.1709
Fax : 216.844.1632
Appointments : 216.844.8500
Outpatient Clinic : Mather Pavillion and Special Immunology Unit


  • B.A. : Christian Albrecht University, Kiel, Germany, 1980-1983
  • M.D. : Julius Maximilian University, Wuerzburg, Germany, 1983-1987
  • Ph.D. equiv : Julius Maximilian University, Wuerzburg, Germany, 1988
  • Internship : Meridia Huron Hospital, Cleveland, Ohio, 1988-1989
  • Residency : MetroHealth Medical Center, Cleveland, Ohio, 1989-1991
  • Fellowship : Case Western Reserve University and MetroHealth Medical Center combined Fellowship Program, Cleveland, Ohio, 1991-1994
  • Postdoctoral Fellowship : Infectious Diseases, Case Western Reserve University, 1994-1996

Clinical Interests

  • Tuberculosis

Research Interests

The focus of my research is the study of the immune response during human tuberculosis (TB); particularly cytokine responses to M. tuberculosis (MTB) and its components and their role in depressed anti-MTB defense mechanisms in the peripheral blood and at the site most commonly affected by TB, the lung.

More recently these studies have focused on identifying the contribution of both T-cell and macrophage apoptosis on host immune reactivity in HIV-infected and -uninfected persons with MTB infection/disease, and on identifying the mediators and mechanisms involved.

MTB infection remains a major source of morbidity and mortality worldwide. Yet immune mechanisms involved in preventing initial MTB infection to activate TB are only incompletly understood. Our previous experience using peripheral blood and lung mononuclear cells from TB patients and healty control subjects indicate that immune mechanisms involved in a lack of control of MTB infection likely are multiple, and involve diverse factors such as overproduction of cytokines associated with intense immune activation (TNF) suppressive cytokines (TGF, IL-10) and increased susceptibility of MTB-responsive T-cells newly recruited to the lung to apoptosis.

Studies currently ongoing in my lab are designed to establish the mechanisms involved in apoptosis of (MTB-responsive) T-cells and to identify whether and how cytokine-mediated pathways are involved in the process.

Selected References

  • Toossi Z, Wu M, Rojas R, Kalsdorf B, Aung H, Hirsch CS, Walrath J, Wolbink A, van Ham M, Silver RF. Induction of serine protease inhibitor 9 by Mycobacterium tuberculosis inhibits apoptosis and promotes survival of infected macrophages. J Infect Dis. 2012 Jan;205(1):144-51. Epub 2011 Nov 16.
  • Toossi Z, Wu M, Hirsch CS, Mayanja-Kizza H, Baseke J, Aung H, Canaday DH, Fujinaga K. Activation of P-TEFb at Sites of Dual HIV/TB Infection, and Inhibition of MTB-Induced HIV Transcriptional Activation by the Inhibitor of CDK9, Indirubin-3'-Monoxime. AIDS Res Hum
  • Toossi Z, Mayanja-Kizza H, Lawn SD, Hirsch CS, Lupo LD, Butera ST. Dynamic variation in the cellular origin of HIV type 1 during treatment of tuberculosis in dually infected subjects. AIDS Res Hum Retroviruses. 2007 Jan;23(1):93-100