Summary auto-generated
This study investigated how rotavirus-specific memory B cells develop in gut-associated lymphoid tissue (GALT) after a single oral immunization of mice with rhesus rotavirus (RRV). Researchers tracked the frequency and location of these memory B cells over time by isolating cells from various lymphoid tissues and stimulating them in culture to measure IgA-secreting antibody responses. While rotavirus-specific memory B cells were initially present in Peyer's patches and spleen 4-8 weeks after immunization, their frequency decreased by 14-18 weeks. Conversely, memory B cell numbers increased in the lamina propria (LP)—the tissue layer beneath the intestinal epithelium—at the later timepoint. This delayed accumulation of memory B cells in the LP correlated with enhanced protection against rotavirus challenge. The findings suggest that memory B cells migrate from secondary lymphoid organs to the intestinal LP over time, and that local presence of these cells in the LP is critical for protective immunity against mucosal rotavirus infection. The work emphasizes that protection depends on memory B cell localization at the infection site rather than their presence in systemic lymphoid tissues.
Key findings
- Rotavirus-specific memory B cells accumulate in the lamina propria between 6-16 weeks after primary oral immunization, while decreasing in Peyer's patches and spleen over the same period.
- Memory B cells in lamina propria were detected only late after immunization (14-18 weeks), not early (4-8 weeks), despite initial presence in secondary lymphoid organs.
- Protection against rotavirus challenge correlated with the frequency of virus-specific memory B cells in the lamina propria rather than their presence in other lymphoid tissues.
- In vitro stimulation of lymphoid cells generated rotavirus-specific IgA-secreting cells only at 5 days post-stimulation, confirming these were secondary effector B cells derived from memory cells.
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Abstract
We found previously that mice inoculated orally with simian rotavirus strain RRV developed virus-specific memory B cell responses 16 weeks after immunization that were greater than those found 6 weeks after immunization. Memory B cell responses were defined as the quantity of virus-specific IgA detected in small intestinal lamina propria (LP) fragment cultures of immunized mice at various intervals after challenge. Enhanced memory B cell responses correlated with enhanced protection against shedding. In order to understand better the delayed onset of rotavirus-specific memory B cell responses, a method was developed to determine the frequencies of rotavirus-specific memory B cells in gut-associated lymphoid tissues (GALT). We found that protection against rotavirus challenge was determined by the frequency of rotavirus-specific memory B cells in GALT LP.