Table 1.
AI4 T cell–induced diabetes in NOD.IFN-γnull mice is blocked by coinfusing recipients with splenocytes from standard NOD mice individually lacking T or B cells, but not both lymphocyte subtypes
| Source of splenocytes coinjected with 1 × 107 NOD.Rag1null.AI4 splenocytes into NOD.IFN-γnull recipients* | Fraction diabetic | Percent diabetic | χ2 P value† |
|---|---|---|---|
| NOD.IFN-γnull | 25/25 | 100 | — |
| NOD | 0/10 | 0 | <0.001 |
| NOD.IgHnull | 0/5 | 0 | <0.001 |
| NOD.TCRαnull | 1/5 | 20 | <0.001 |
| NOD.CD8null | 0/5 | 0 | <0.001 |
| NOD CD8-depleted | 0/4 | 0 | <0.001 |
| NOD CD4-depleted | 0/4 | 0 | <0.001 |
| NOD CD8- and CD4-depleted | 0/4 | 0 | <0.001 |
| NOD CD8-, CD4-, and B cell–depleted | 8/10 | 80 | 0.05 > P > 0.02 |
| NOD.Rag1null | 5/5 | 100 | NS |
| NOD.scid | 9/10 | 90 | NS |
*Recipients were monitored for diabetes development for 3 weeks after adoptive transfer of splenocytes.
†P values from χ2 analyses comparing the frequency of diabetes between AI4 splenocyte–infused NOD.IFN-γnull mice coinjected with NOD.IFN-γnull splenocytes and splenocytes from other sources.