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. 2011 May 10;6(5):e14796. doi: 10.1371/journal.pone.0014796

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This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

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The simulations here have been generated using the scaled version of the two-clone model (3a)–(3g) (see Supplementary Material S1). The scaled levels of (A1–C1) the two low-avidity Auto-Ag-specific subclones: (black/solid) and (black/dashed); (A2–C2) the two high-avidity Auto-Ag-specific subclones: (gray/solid) and (gray/dashed); (A3–C3) beta cells (black solid); and (A4–C4) immunoglobulin specific to: Auto-Ag, (black), and auto-Ag, (gray), are shown. Dotted lines in panels (A3–C3) correspond to the 30% critical beta-cell number (threshold) required for preventing clinical symptoms of T1D (staying insulin-independent). Model responses to variations in the value of (while keeping , and fixed) are simulated to determine the effects of the lower avidity Auto-Ag-specific subclone, , on disease progression. In the upper panels (A1–A4) ; in the middle panels (B1–B4) ; and in the lower panels (C1–C4) . The subclone in panel (A2) has the same parameter values as the “standard clone” used in Fig. 5 (white circle). Notice that the levels of autoantibodies, shown in panels (A4–C4), corresponding to the higher avidity Auto-Ag-specific subclones (gray lines), become detectable earlier than those corresponding to the lower avidity Auto-Ag-specific subclones (black lines). Also, decreasing the level of avidity of alone in the bottom row (C1–C4), increases the level of beta-cell destruction by reaching steady state level below the 30% threshold (panel (C3)).

Inline graphic — The simulations here have been generated using the scaled version of the two-clone model (3a)–(3g) (see Supplementary Material S1). The scaled levels of (A1–C1) the two low-avidity Auto-Ag-specific subclones: (black/solid) and (black/dashed); (A2–C2) the two high-avidity Auto-Ag-specific subclones: (gray/solid) and (gray/dashed); (A3–C3) beta cells (black solid); and (A4–C4) immunoglobulin specific to: Auto-Ag, (black), and auto-Ag, (gray), are shown. Dotted lines in panels (A3–C3) correspond to the 30% critical beta-cell number (threshold) required for preventing clinical symptoms of T1D (staying insulin-independent). Model responses to variations in the value of (while keeping , and fixed) are simulated to determine the effects of the lower avidity Auto-Ag-specific subclone, , on disease progression. In the upper panels (A1–A4) ; in the middle panels (B1–B4) ; and in the lower panels (C1–C4) . The subclone in panel (A2) has the same parameter values as the “standard clone” used in Fig. 5 (white circle). Notice that the levels of autoantibodies, shown in panels (A4–C4), corresponding to the higher avidity Auto-Ag-specific subclones (gray lines), become detectable earlier than those corresponding to the lower avidity Auto-Ag-specific subclones (black lines). Also, decreasing the level of avidity of alone in the bottom row (C1–C4), increases the level of beta-cell destruction by reaching steady state level below the 30% threshold (panel (C3)).