Table 3.

Comparative clinical features of dominant-negative PSMB10 disease, dominant-negative PSMB9 disease, POMP deficiency (PRAID), and autosomal recessive PRAAS

Dominant-negative PSMB10 (10 patients)Dominant-negative PSMB9 (2 patients)POMP deficiency (5 patients)Autosomal recessive PRAAS (<100 patients)
Inheritance De novo, heterozygous De novo, heterozygous De novo, heterozygous Autosomal recessive 
Age at onset Neonatal/infancy Neonatal/infancy Infancy Infancy/early childhood 
Systemic inflammation − (not prominent) ++ ++ ++ 
Liver involvement +++ (frequent, severe VOD, liver failure, and high mortality) ++ (early cirrhosis, CMV-triggered hepatitis, and fatal liver failure) + (mild-moderate, rarely severe) + (mild-moderate, hepatomegaly common, failure rare) 
Gastrointestinal involvement ++ (mild to severe enteropathy) ​ ​ ​ 
Pulmonary hypertension − ++ − − 
Skin involvement Erythroderma and severe atopic dermatitis Erythroderma and neonatal rash Neutrophilic dermatosis Panniculitis, lipodystrophy and chronic rash 
Lipodystrophy − − − ++ 
Muscle/Joint involvement − Myositis − Myositis, muscle atrophy, and joint contractures 
Infections ++, recurrent opportunistic infections − ++, recurrent opportunistic infections +/− 
Immunological Features Severe SCID/CID T cell lymphopenia and CD8+ T cell loss CID Mild to moderate lymphopenia 
​ Profound T and B cell lymphopenia ​ T and B cell lymphopenia Pancytopenia (variable) 
​ Low naïve T cell (variable) ​ ​ Hypergammaglobulinemia 
​ Hypogammaglobulinemia ​ ​ ​ 
IFN-I signature Normal in 2 tested patients High High in 1 High 
​ ​ ​ Normal in 1 (under treatment) ​ 
JAK-inhibitor Not tested Efficient on pulmonary hypertension and autoinflammation (1 patient) Might control autoinflammation increased risk of infection Indicated for autoinflammation 
HSCT outcome Very high morbi-mortality 1 patient transplanted and cured 2 patients transplanted and cured 1 PSMB4-deficient patient and cured 
Dominant-negative PSMB10 (10 patients)Dominant-negative PSMB9 (2 patients)POMP deficiency (5 patients)Autosomal recessive PRAAS (<100 patients)
Inheritance De novo, heterozygous De novo, heterozygous De novo, heterozygous Autosomal recessive 
Age at onset Neonatal/infancy Neonatal/infancy Infancy Infancy/early childhood 
Systemic inflammation − (not prominent) ++ ++ ++ 
Liver involvement +++ (frequent, severe VOD, liver failure, and high mortality) ++ (early cirrhosis, CMV-triggered hepatitis, and fatal liver failure) + (mild-moderate, rarely severe) + (mild-moderate, hepatomegaly common, failure rare) 
Gastrointestinal involvement ++ (mild to severe enteropathy) ​ ​ ​ 
Pulmonary hypertension − ++ − − 
Skin involvement Erythroderma and severe atopic dermatitis Erythroderma and neonatal rash Neutrophilic dermatosis Panniculitis, lipodystrophy and chronic rash 
Lipodystrophy − − − ++ 
Muscle/Joint involvement − Myositis − Myositis, muscle atrophy, and joint contractures 
Infections ++, recurrent opportunistic infections − ++, recurrent opportunistic infections +/− 
Immunological Features Severe SCID/CID T cell lymphopenia and CD8+ T cell loss CID Mild to moderate lymphopenia 
​ Profound T and B cell lymphopenia ​ T and B cell lymphopenia Pancytopenia (variable) 
​ Low naïve T cell (variable) ​ ​ Hypergammaglobulinemia 
​ Hypogammaglobulinemia ​ ​ ​ 
IFN-I signature Normal in 2 tested patients High High in 1 High 
​ ​ ​ Normal in 1 (under treatment) ​ 
JAK-inhibitor Not tested Efficient on pulmonary hypertension and autoinflammation (1 patient) Might control autoinflammation increased risk of infection Indicated for autoinflammation 
HSCT outcome Very high morbi-mortality 1 patient transplanted and cured 2 patients transplanted and cured 1 PSMB4-deficient patient and cured 

HLH: hemophagocytic lymphohistiocytosis; PRAID: POMP-related autoinflammation and immune dysregulation.

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