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Infection and Immunity, October 2007, p. 4933-4941, Vol. 75, No. 10
0019-9567/07/$08.00+0     doi:10.1128/IAI.00705-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

T-Cell-Independent Humoral Immunity Is Sufficient for Protection against Fatal Intracellular Ehrlichia Infection{triangledown}

Constantine Bitsaktsis,1 Bisweswar Nandi,1 Rachael Racine,2 Katherine C. MacNamara,1 and Gary Winslow1,2*

Wadsworth Center, New York State Department of Health, P.O. Box 22002, Albany, New York 12201-2002,1 The Department of Biomedical Sciences, School of Public Health, University at Albany, Albany, New York 12201-05092

Received 24 May 2007/ Returned for modification 27 June 2007/ Accepted 18 July 2007

Although humoral immunity has been shown to contribute to host defense during intracellular bacterial infections, its role has generally been ancillary. Instead, CD4 T cells are often considered to play the dominant role in protective immunity via their production of type I cytokines. Our studies of highly pathogenic Ehrlichia bacteria isolated from Ixodes ovatus (IOE) reveal, however, that this paradigm is not always correct. Immunity to IOE infection can be induced by infection with a closely related weakly pathogenic ehrlichia, Ehrlichia muris. Type I cytokines (i.e., gamma interferon, tumor necrosis factor alpha, and interleukin-12) were not necessary for E. muris-induced immunity. In contrast, humoral immunity was essential, as shown by the fact that E. muris-infected B-cell-deficient mice were not protected from IOE challenge and because E. muris immunization was effective in CD4-, CD8-, and major histocompatibility complex (MHC) class II-deficient mice. Immunity was unlikely due to nonspecific inflammation, as prior infection with Listeria monocytogenes did not induce immunity to IOE. Antisera from both wild-type and MHC-II-deficient mice provided at least partial resistance to challenge infection, and protection could also be achieved following transfer of total, but not B-cell-depleted, splenocytes obtained from E. muris-immunized mice. The titers of class-switched antibodies in immunized CD4 T-cell- and MHC class II-deficient mice, although lower than those observed in immunized wild-type mice, were significant, indicating that E. muris can induce class switch recombination in the absence of classical T-cell-mediated help. These studies highlight a major protective role for classical T-cell-independent humoral immunity during an intracellular bacterial infection.

* Corresponding author. Mailing address: Wadsworth Center, 120 New Scotland Avenue, Albany, NY 12208. Phone: (518) 473-2795. Fax: (518) 486-9858. E-mail: gary.winslow{at}wadsworth.org

{triangledown} Published ahead of print on 30 July 2007.

Editor: R. P. Morrison

Infection and Immunity, October 2007, p. 4933-4941, Vol. 75, No. 10
0019-9567/07/$08.00+0     doi:10.1128/IAI.00705-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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