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Journal of Virology, October 2004, p. 10967-10976, Vol. 78, No. 20
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.20.10967-10976.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Maturation and Trafficking Markers on Rotavirus-Specific B Cells during Acute Infection and Convalescence in Children

María C. Jaimes,^1, Olga L. Rojas,^2, Eric J. Kunkel,³ Nicole H. Lazarus,³ Dulce Soler,⁴ Eugene C. Butcher,³ Dorsey Bass,⁵ Juana Angel,² Manuel A. Franco,^2, and Harry B. Greenberg^1*,

Departments of Medicine, Microbiology, and Immunology,¹ Laboratory of Immunology and Vascular Biology, Department of Pathology,³ Division of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Stanford University School of Medicine, and Veterans Administration Palo Alto Health Care System, Stanford, California,⁵ Instituto de Genética Humana, Pontificia Universidad Javeriana, Bogotá, Colombia,² Inflammation Department, Millennium Pharmaceuticals, Cambridge, Massachusetts⁴

Received 19 April 2004/ Accepted 27 May 2004

We have previously studied B cells, from people and mice, that express rotavirus-specific surface immunoglobulin (RV-sIg) by flow cytometry with recombinant virus-like particles that contain green fluorescent protein. In the present study we characterized circulating B cells with RV-sIg in children with acute and convalescent infection. During acute infection, circulating RV-sIgD^– B cells are predominantly large, CD38^high, CD27^high, CD138^+/–, CCR6^–, 4ß7⁺, CCR9⁺, CCR10⁺, cutaneous lymphocyte antigen-negative (CLA^–), L-selectin^int/–, and sIgM⁺, sIgG^–, sIgA^+/– lymphocytes. This phenotype likely corresponds to gut-targeted plasma cells and plasmablasts. During convalescence the phenotype switches to small and large lymphocytes, CD38^int/–, CD27^int/–, CCR6⁺, 4ß7^+/–, CCR9^+/– and CCR10^–, most likely representing RV-specific memory B cells with both gut and systemic trafficking profiles. Of note, during acute RV infection both total and RV-specific murine IgM and IgA antibody-secreting cells migrate efficiently to CCL28 (the CCR10 ligand) and to a lesser extent to CCL25 (the CCR9 ligand). Our results show that CCR10 and CCR9 can be expressed on IgM as well as IgA antibody-secreting cells in response to acute intestinal infection, likely helping target these cells to the gut. However, these intestinal infection-induced plasmablasts lack the CLA homing receptor for skin, consistent with mechanisms of differential CCR10 participation in skin T versus intestinal plasma cell homing. Interestingly, RV memory cells generally lack CCR9 and CCR10 and instead express CCR6, which may enable recruitment to diverse epithelial sites of inflammation.

M.C.J. and O.L.R. contributed equally to the work presented, and M.A.F. and H.B.G. contributed equally as senior authors.

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