IFNG genotypes and LPD development in hu PBL-SCID mice
. | . | Intermediate/late . | . | |
|---|---|---|---|---|
| Genotype . | Rapid LPD, % . | LPD, % . | No LPD, % . | |
| A/A* | 58.3 | 7.1 | 26.1 | |
| T/A | 41.7 | 50.0 | 39.1 | |
| T/T† | 0 | 42.9 | 34.8 | |
. | . | Intermediate/late . | . | |
|---|---|---|---|---|
| Genotype . | Rapid LPD, % . | LPD, % . | No LPD, % . | |
| A/A* | 58.3 | 7.1 | 26.1 | |
| T/A | 41.7 | 50.0 | 39.1 | |
| T/T† | 0 | 42.9 | 34.8 | |
Three to 5 SCID mice were injected per PBL donor, and all mice were engrafted, as evidenced by more than 750 μg/mL human IgG in the sera. For rapid LPD, n = 12; for intermediate/late LPD, n = 14; and for no LPD, n = 23.
A/A genotype is significantly more prevalent in the rapid LPD group, P = .0144.
The presence of the A allele (A/A + T/A) is significantly more prevalent in the rapid LPD group, P = .0257.