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American Association of Immunologists, The Journal of Immunology, 8(161), p. 4227-4235, 1998

DOI: 10.4049/jimmunol.161.8.4227

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The memory B cell subset responsible for the secretory IgA response and protective humoral immunity to rotavirus expresses the intestinal homing receptor, α4β7

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

AbstractInfection 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 α4β7 integrin on lymphocytes with the vascular mucosal addressin cell adhesion molecule-1. To determine whether B cell memory for RV correlates with α4β7 expression, we transferred sorted B220+ phenotypically defined memory (IgD−α4β7high and IgD− α4β7−) and naive (IgD+α4β7+) splenocytes into recombination-activating gene-2 knockout mice (B and T cell-deficient) that were chronically infected with RV. Only mice receiving α4β7high memory (IgD−) B cells produced RV-specific IgA in the stool, cleared the virus, and were immune to reinfection. α4β7high (but not α4β7−) memory B cells from donors boosted as much as 7 mo previously also cleared the virus, indicating that α4β7high memory B cells maintain long term functional immunity to RV. Although only α4β7high memory cells provided mucosal immunity, α4β7− 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, α4β7.