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CD11c Expression Identifies a Population of Extrafollicular Antigen-Specific Splenic Plasmablasts Responsible for CD4 T-Independent Antibody Responses during Intracellular Bacterial Infection¹

Rachael Racine, Madhumouli Chatterjee^* and Gary M. Winslow^2,*,

^* Wadsworth Center, New York State Department of Health, Albany, NY 12201; and Department of Biomedical Sciences, School of Public Health, University, Albany, NY 12201

Although T-independent immunity is known to be generated against bacterial capsular and cell wall polysaccharides expressed by a number of bacterial pathogens, it has not been studied in depth during intracellular bacterial infections. Our previous study demonstrated that Ehrlichia muris, an obligate intracellular tick-borne pathogen, generates protective classical TI responses in CD4 T cell-deficient C57BL/6 mice. We found that E. muris T-independent immunity is accompanied by the expansion of a very large extrafollicular spleen population of CD11c^low-expressing plasmablasts that exhibit characteristics of both B-1 and marginal zone B cells. The plasmablasts comprised up to 15% of the total spleen lymphocytes and 70% of total spleen IgM^highIgD^low cells during peak infection in both wild-type and MHC class II-deficient mice. The CD11c^low cells exhibited low surface expression of B220, CD19, and CD1d, high expression of CD11b, CD43, but did not express CD5. Approximately 50% of the CD11c^low cells also expressed CD138. In addition to CD11b and CD11c, the plasmablasts expressed the β₁ (CD29) and 4 (CD49d) integrins, as well as the chemokine receptor CXCR4, molecules which may play roles in localizing the B cells extrafollicular region of the spleen. During peak infection, the CD11c^low cells accounted for the majority of the IgM-producing splenic B cells and nearly all of the E. muris outer membrane protein-specific IgM-secreting cells. Thus, during this intracellular bacterial infection, CD11c expression identifies a population of Ag-specific spleen plasmablasts responsible for T-independent Ab production.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by U.S. Public Health Service Grant R01AI47963-01 (to G.M.W.).

² Address correspondence and reprint requests to Dr. Gary Winslow, Wadsworth Center, 120 New Scotland Avenue, Albany, NY 12208. E-mail address: gary.winslow{at}wadsworth.org

³ Abbreviations used in this paper: TI, T independent; MZ, marginal zone; HME, human monocytotropic ehrlichiosis; IOE, Ixodes ovatus ehrlichia; OMP, outer membrane protein; rt, room temperature; DC, dendritic cell; MFI, mean fluorescence intensity; FO, follicular.