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Infection and Immunity, February 2004, p. 966-971, Vol. 72, No. 2
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.2.966-971.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Mechanisms of Immunity to Ehrlichia muris: a Model of Monocytotropic Ehrlichiosis

Hui-Min Feng and David H. Walker*

Department of Pathology, University of Texas Medical Branch, Galveston, Texas 77555

Received 11 August 2003/ Returned for modification 16 September 2003/ Accepted 13 November 2003

Ehrlichia species can cause life-threatening infections or chronic persistent infections. Mechanisms of protective immunity were examined in an Ehrlichia muris mouse model of monocytotropic ehrlichiosis. C57BL/6 mice possessed strong genetic resistance to E. muris of an undetermined mechanism. CD8 T lymphocytes were particularly important, as revealed by 81% fatalities for E. muris-infected, major histocompatibility complex class I gene knockout mice compared with no deaths for wild-type C3H mice. Moreover, 80% of C3H mice depleted of CD8 and CD4 cells died of E. muris infection compared with only 44% of CD4 cell-depleted mice. CD8 T lymphocytes were demonstrated for the first time in an Ehrlichia infection to exhibit cytotoxic T-lymphocyte activity against Ehrlichia-infected target cells. Both gamma interferon and tumor necrosis factor were shown to play synergistic roles in protective immunity in vivo for the first time, as demonstrated by 75% fatalities when both cytokines were neutralized compared with minimal mortality when they were depleted separately. Passive transfer of antibodies, but not Fab fragments, to E. muris protected C3H/SCID mice against lethal infection. The mechanism of increased susceptibility (22% lethality) of C57BL/6 major histocompatibility complex class II gene knockout mice and CD4 cell-depleted C3H mice (i.e., through a gamma interferon or antibody mechanism), as well as the more important role of CD8 T lymphocytes (in the form of cytotoxic T-lymphocyte activity and/or gamma interferon production), remains to be elucidated. Protective immunity against monocytotropic E. muris is mediated by a combination of CD8 and CD4 T lymphocytes, gamma interferon, tumor necrosis factor alpha, and antibodies.

* Corresponding author. Mailing address: Department of Pathology, Center for Biodefense and Emerging Infectious Diseases, 301 University Blvd., Keiller Bldg., Galveston, TX 77555-0609. Phone: (409) 772-2856. Fax: (409) 772-1850. E-mail: dwalker{at}utmb.edu.

Editor: W. A. Petri, Jr.

Infection and Immunity, February 2004, p. 966-971, Vol. 72, No. 2
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.2.966-971.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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