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*
Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University, and
Departments of Medicine, Microbiology, and Immunology, Stanford University School of Medicine, Stanford, CA 94305; and
Veterans Affairs Palo Alto Health Care System, Palo Alto, CA 94304
The intestinal homing receptor,
4
7, helps target lymphocytes to Peyers
patches (PP) and intestinal lamina propria (ILP). We have previously
shown that protective immunity to rotavirus (RV), an intestinal
pathogen, resides in memory B cells expressing
4
7. In this study, using a novel FACS
assay, we have directly studied the phenotype of B cells that express
surface RV-specific Ig during the in vivo RV immune response. During
primary infection, RV-specific B cells first appear as large
IgD-B220low
4
7-
and
4
7+ cells (presumptive
extrafollicular, Ab-secreting B cells), and then as large and small
IgD-B220high
4
7-
cells (presumptive germinal center B cells). The appearance of B cells
with the phenotype of large
IgD-B220low
4
7+
cells in PP and most notably in mesenteric lymph nodes coincides with
the emergence of RV-specific Ab-secreting cells (ASC) in the ILP. Thus,
these B lymphocytes are good candidates for the migratory population
giving rise to the RV-specific ASC in the ILP. RV-specific long-term
memory B cells preferentially accumulate in PP and express
4
7. Nine months after infection most
RV-specific IgA ASC are found in PP and ILP and at lower frequency in
bone marrow and spleen. This study is the first to follow changes in
tissue-specific homing receptor expression during Ag-specific B cell
development in response to a natural host, tissue-specific pathogen.
These results show that
4
7 is tightly
regulated during the Ag-specific B cell response to RV and is expressed
concurrently with the specific migration of memory and effector B cells
to intestinal tissues.
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