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. 2000 Jul 3;192(1):87–98. doi: 10.1084/jem.192.1.87

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© 2000 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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graphic file with name JEM000065.f7ab.jpg — Persistent clonal loss of V_HT15 and clan III–expressing peritoneal B-1 cells. In each multigroup study, naive, SpA- or control protein-treated mice were included, with comparisons to naive BALB/c and C57BL/6 mice. Mice were treated as neonates, and then evaluated 7–21 wk later in microfluorimetric assays. Representative results from studies of T15i mice (A) peritoneal cavity and (B) splenic mononuclear cells are displayed. For these analyses, gates were set so that <0.8% of C57BL/6 (IgM^b)B220⁺ cells were reactive with the IgM^a-specific reagent. Representative results are shown from the (C) peritoneal cells of matched groups of TCR-β^2/2δ^2/2 mice, evaluated 16 wk after the last exposure. In these results, control mice were treated with HEL, with equivalent findings in control β-galactosidase–treated mice (not shown). For each B cell subset, the IgM^a or LJ-26 reactivity was used to derive the percentages representative of clan VHIII–expressing B cells.

graphic file with name JEM000065.f7c.jpg — Persistent clonal loss of V_HT15 and clan III–expressing peritoneal B-1 cells. In each multigroup study, naive, SpA- or control protein-treated mice were included, with comparisons to naive BALB/c and C57BL/6 mice. Mice were treated as neonates, and then evaluated 7–21 wk later in microfluorimetric assays. Representative results from studies of T15i mice (A) peritoneal cavity and (B) splenic mononuclear cells are displayed. For these analyses, gates were set so that <0.8% of C57BL/6 (IgM^b)B220⁺ cells were reactive with the IgM^a-specific reagent. Representative results are shown from the (C) peritoneal cells of matched groups of TCR-β^2/2δ^2/2 mice, evaluated 16 wk after the last exposure. In these results, control mice were treated with HEL, with equivalent findings in control β-galactosidase–treated mice (not shown). For each B cell subset, the IgM^a or LJ-26 reactivity was used to derive the percentages representative of clan VHIII–expressing B cells.