Table 2. Analysis of a challenging sample cohort with ADAP assay.
Suspected T1D | Control | SLE | HG | ||||||||
---|---|---|---|---|---|---|---|---|---|---|---|
GAD Ab | |||||||||||
Rad + | Rad - | Rad + | Rad - | Rad + | Rad - | Rad + | Rad - | ||||
ADAP+ | 7 | 2 | 0 | 0 | 0 | 0 | 0 | 3* | |||
ADAP- | 0 | 11 | 0 | 20 | 0 | 6 | 0 | 11 | |||
IA-2 Ab | |||||||||||
Rad + | Rad - | Rad + | Rad - | Rad + | Rad - | Rad + | Rad - | ||||
ADAP+ | 6 | 1 | 0 | 0 | 0 | 0 | 0 | 0 | |||
ADAP- | 0 | 13 | 0 | 20 | 0 | 6 | 0 | 14 | |||
INS Ab | |||||||||||
Rad + | Rad - | Rad + | Rad - | Rad + | Rad - | Rad + | Rad - | ||||
ADAP+ | 9 | 4 | 0 | 0 | 0 | 0 | 0 | 0 | |||
ADAP- | 0 | 7 | 0 | 20 | 0 | 6 | 0 | 14 |
A total of 20 T1D, 20 controls, 6 systemic lupus erythematosus (SLE) and 14 hyperglobulinemia (HG) serum samples were included in this cohort to determine the off-target propensity of ADAP in a population with autoimmune and/or inflammatory disorders. Only 3 HG patients showed GAD autoantibodies by ADAP (*The HG samples have not been tested by radioassays, and were presumed to be radioassay negative). This cohort was analyzed with blinding. Radioassay was abbreviated as Rad.