期刊
JOURNAL OF VIROLOGY
卷 78, 期 20, 页码 10967-10976出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.78.20.10967-10976.2004
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资金
- NHLBI NIH HHS [P50 HL067674, HL 67674, P01 HL067674] Funding Source: Medline
- NIAID NIH HHS [R01 AI 21362-20, R01 AI021362, R37 AI047822, AI 47822, R21 AI047822, R01 AI047822] Funding Source: Medline
- NIDDK NIH HHS [P30 DK056339, DK 56339] Funding Source: Medline
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(-), alpha4beta7(+), 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(+), alpha4beta7(+/-) 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 CIA 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 epithellial sites of inflammation.
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