The designation "AGL28" refers to a patient code in a clinical cohort study investigating anti-PLIN1 autoantibodies in AGL (Table 2, ). AGL28 was classified under the autoimmune variety of lipodystrophy and exhibited IgG-type autoantibodies with the following characteristics:
IgG subclass: IgG3
Light chains: κ + λ
IgG autoantibody titer: 421.4 AU/mL
This patient’s serum showed reactivity against the PLIN1 epitope 383–403, a key region recognized by anti-PLIN1 autoantibodies in AGL .
Anti-PLIN1 autoantibodies are a diagnostic biomarker for AGL, particularly in autoimmune and panniculitis-associated subtypes .
These autoantibodies target intracellular lipid-droplet proteins, leading to adipocyte destruction and systemic metabolic dysfunction.
Data from the AGL cohort (n=20) revealed the following patterns for anti-PLIN1 autoantibodies :
Parameter | IgG-Positive Patients (n=19) | IgM-Positive Patients (n=6) |
---|---|---|
Median disease duration | 13.43 years | 8.82 years |
Fat mass reduction | 75% exhibited reduced adiposity | 66.7% exhibited reduced adiposity |
Light chain usage | 75% κ + λ; 25% κ-only | 100% κ + λ |
While AGL28 itself is not a therapeutic antibody, the study highlights:
Clinical relevance: Anti-PLIN1 autoantibodies correlate with metabolic complications such as hypertriglyceridemia and diabetes .
Treatment gaps: No targeted therapies exist for AGL; management focuses on metabolic symptom relief (e.g., leptin replacement) .