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4ß71
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*
Laboratory of Immunology and Vascular Biology, Department of Pathology, and
Digestive Disease Center, Stanford University, Stanford, CA 94305;
Departments of Medicine and Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305; and
§
Veterans Affairs Palo Alto Health Care System, Palo Alto, CA 94304
Infection of mice with murine rotaviruses induces life-long
immunity, characterized by high levels of IgA in the intestine and
large numbers of rotavirus (RV)-specific Ab-secreting cells in
gut-associated lymphoid tissues. Lymphocyte trafficking into
gut-associated lymphoid tissues is mediated by interaction of the
4ß7 integrin on lymphocytes with the
vascular mucosal addressin cell adhesion molecule-1. To determine
whether B cell memory for RV correlates with
4ß7 expression, we transferred sorted
B220+ phenotypically defined memory
(IgD-4ß7high and
IgD- 4ß7-) and
naive (IgD+4ß7+)
splenocytes into recombination-activating gene-2 knockout mice (B and T
cell-deficient) that were chronically infected with RV. Only mice
receiving 4ß7high memory
(IgD-) B cells produced RV-specific IgA in the stool,
cleared the virus, and were immune to reinfection.
4ß7high (but not
4ß7-) memory B cells from
donors boosted as much as 7 mo previously also cleared the virus,
indicating that 4ß7high memory
B cells maintain long term functional immunity to RV. Although only
4ß7high memory cells provided
mucosal immunity, 4ß7- cells
from recently boosted donor animals could generate RV-specific serum
IgG, but, like naive (IgD+) B cells, were unable to induce
viral clearance even 60 days after cell transfer. These data indicate
that protective immunity for an intestinal pathogen, RV, resides in
memory phenotype B cells expressing the intestinal homing receptor,
4ß7.
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