Table 2.

Indications for HSCT in PID.

HSCT curative	HSCT partially curative	HSCT controversial
SCID	Cartilage Hair Hypoplasia	CVID
CID∧	PGM3 deficiency	Agammaglobulinemia
CGD	STAT1-GOF	Complement deficiencies (other than C1q deficiency)
DOCK8 deficiency	STAT3- GOF	DGS
DOCK2 deficiency	Severe congenital neutropenia	IKBA deficiency
IPEX	ADA2 deficiency	NEMO deficiency
WAS	CIQ deficiency
WIP deficiency	CD25 deficiency
ARPC1B deficiency	IL-10 deficiency
CD40 ligand deficiency	IL-10 Receptor deficiency
CD40 deficiency	DNA double-strand break repair disorders
XLP1, XLP2
APDS
MHC Class II deficiency
AD Hyper IgE syndrome
CTLA4 haploinsufficiency
LRBA deficiency
Familial HLH types 1–5
GATA2 deficiency
RAB27A deficiency
LAD I
Reticular Dysgenesis

^∧Depending on the clinical and immunological phenotype. SCID, severe combined immunodeficiency; CID, combined immunodeficiency; CGD; chronic granulomatous disease; DOCK8, dedicator of cytokinesis 8; DOCK2, dedicator of cytokinesis 2; IPEX, immune dysregulation, polyendocrinopathy, enteropathy, X-linked; WAS, Wiskott-Aldrich syndrome; WIP, WASP interacting protein; ARPC1B, actin related protein 2/3 complex subunit 1B; XLP1, X-linked lymphoproliferative disease 1; XLP2, X-linked lymphoproliferative disease 2; APDS, activated PI3K delta syndrome; MHC, major histocompatibility complex; AD, autosomic dominant; CTLA-4, cytotoxic T-lymphocyte-associated protein 4; LRBA, lipopolysaccharide (LPS)-Responsive and Beige-like Anchor protein; HLH, hemophagocytic lymphohistiocytosis; GATA2, GATA binding protein 2; RAB27A, member RAS oncogene family; LAD, leukocyte adhesion deficiency; PGM3, phosphoacetylglucosamine mutase; STAT1, signal transducer and activator of transcription 1; STAT2, signal transducer and activator of transcription 2; GOF, gain of function; ADA2, adenosine deaminase 2; CVID, common variable immune deficiency; DGS, DiGeorge syndrome; NEMO, nuclear factor-kappa B essential modulator.