Table 4.

Genetic conditions associated with predisposition to HLH

Selected mechanism(s) of HLH predisposition
Familial HLH  
 PRF1 Defective lymphocyte granule–mediated cytotoxicity 
 UNC13D Defective lymphocyte granule–mediated cytotoxicity 
 STX11 Defective lymphocyte granule–mediated cytotoxicity 
 STXBP2 Defective lymphocyte granule–mediated cytotoxicity 
Pigmentary disorders associated with HLH  
 RAB27A Defective lymphocyte granule–mediated cytotoxicity 
 LYST Defective lymphocyte granule–mediated cytotoxicity 
 AP3B1 Defective lymphocyte granule–mediated cytotoxicity 
XLP-1 and XLP-2  
 SH2D1A Defective 2B4-mediated cytotoxicity; defective T-cell restimulation–induced cell death; absent iNKT cells 
 XIAP Dysregulated NLRP3 inflammasome function; increased effector cell susceptibility to cell death 
 NLRC4 Constitutively active NLRC4 inflammasome function 
 CDC42 Defective formation of actin-based structures; defective proliferation, migration, and cytotoxicity; increased IL-1β and Il-18 production 
EBV susceptibility disorders  
 MAGT1 Defective Mg++ transporter; low NKG2D, defective cytotoxicity 
 ITK Defective tyrosine kinase function; defective cytotoxic T-cell expansion and cytolytic capacity; decreased iNKT cells 
 CD27 CD27 expressed on T cells participates in costimulatory signaling, interacts with CD70; required for normal T-cell proliferation and triggering of cytotoxicity against EBV-infected B cells; decreased iNKT cells 
 CD70 CD70 expressed by EBV-infected B cells interacts with CD27 on T cells; required for normal expansion and cytotoxicity of the T cells; decreased NKG2D, 2B4; decreased iNKT cells 
 CTPS1 Enzyme involved in de novo synthesis of cytidine nucleotide triphosphate (CTP) (critical precursor of nucleic acid metabolism); deficiency leads to impaired proliferation; decreased iNKT cells 
 RASGRP1 Activates RAS, which leads to MAPK pathway activation; defects in T-cell activation, proliferation, and migration; decreased cytotoxicity; decreased iNKT cells 
Selected mechanism(s) of HLH predisposition
Familial HLH  
 PRF1 Defective lymphocyte granule–mediated cytotoxicity 
 UNC13D Defective lymphocyte granule–mediated cytotoxicity 
 STX11 Defective lymphocyte granule–mediated cytotoxicity 
 STXBP2 Defective lymphocyte granule–mediated cytotoxicity 
Pigmentary disorders associated with HLH  
 RAB27A Defective lymphocyte granule–mediated cytotoxicity 
 LYST Defective lymphocyte granule–mediated cytotoxicity 
 AP3B1 Defective lymphocyte granule–mediated cytotoxicity 
XLP-1 and XLP-2  
 SH2D1A Defective 2B4-mediated cytotoxicity; defective T-cell restimulation–induced cell death; absent iNKT cells 
 XIAP Dysregulated NLRP3 inflammasome function; increased effector cell susceptibility to cell death 
 NLRC4 Constitutively active NLRC4 inflammasome function 
 CDC42 Defective formation of actin-based structures; defective proliferation, migration, and cytotoxicity; increased IL-1β and Il-18 production 
EBV susceptibility disorders  
 MAGT1 Defective Mg++ transporter; low NKG2D, defective cytotoxicity 
 ITK Defective tyrosine kinase function; defective cytotoxic T-cell expansion and cytolytic capacity; decreased iNKT cells 
 CD27 CD27 expressed on T cells participates in costimulatory signaling, interacts with CD70; required for normal T-cell proliferation and triggering of cytotoxicity against EBV-infected B cells; decreased iNKT cells 
 CD70 CD70 expressed by EBV-infected B cells interacts with CD27 on T cells; required for normal expansion and cytotoxicity of the T cells; decreased NKG2D, 2B4; decreased iNKT cells 
 CTPS1 Enzyme involved in de novo synthesis of cytidine nucleotide triphosphate (CTP) (critical precursor of nucleic acid metabolism); deficiency leads to impaired proliferation; decreased iNKT cells 
 RASGRP1 Activates RAS, which leads to MAPK pathway activation; defects in T-cell activation, proliferation, and migration; decreased cytotoxicity; decreased iNKT cells 

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