Warsaw Genomics
Genetic test Frequently chosen

Primary immunodeficiency syndromes

CAP & EMQN quality control
Price 615 EUR 31 days from sample registration in laboratory 354 genes Sample Cheek swab or Venous blood or DNA
Genetic testing with clinical consultation at Warsaw Genomics
~100 000
genomes in our reference database
CAP & EMQN
quality control
In-house
our own laboratory, full control
RODO
genetic data encrypted & protected

What's included in the price

  • NGS sequencing — analysis of the full coding sequence
  • In-house result interpretation by our own team
  • Material collection / delivery per instructions
  • Result available online in the patient portal (PDF)

A consultation with a clinical geneticist is available as a separate service. See the clinic

About this test

Primary immunodeficiencies (PID) constitute a group of over 300 diseases entities with a varied clinical picture, whose pathophysiology may concern each component of the nonspecific and specific immune response.

The most common symptoms are usually severe, recurring infections, with no results despite the use of antibiotics. The symptoms of primary immunodeficiencies are usually found in infants and children. PID occurs with a frequency of 1 in 2,000-3,000.

Genes analysed (354)

Gene Inheritance Associated condition
ACD — —
ACP5 autosomal recessive Spondyloenchondrodysplasia with immune dysregulation
ACTB autosomal dominant —
ADA autosomal recessive Severe combined immunodeficiency, autosomal recessive, T cell-negative, B cell-negative, NK cell-negative, due to adenosine deaminase deficiency
ADAM17 — —
ADAR AD/AR Aicardi-Goutieres syndrome 1, Dyschromatosis symmetrica hereditaria 1
AICDA — —
AIRE AR/AD Autoimmune polyendocrinopathy syndrome , type I, with or without reversible metaphyseal dysplasia
AK2 autosomal recessive —
ALPI — —
AP3B1 autosomal recessive Hermansky-Pudlak syndrome 6
ARHGEF1 — —
ARPC1B — —
ATM AD/AR Ataxia-telangiectasia, Breast cancer
ATP6AP1 — —
BACH2 — —
BCL10 — —
BCL11B — —
BLM autosomal recessive Bloom syndrome
BLNK — —
BTK X-linked Agammaglobulinemia, X-linked, Isolated growth hormone deficiency, type III, with agammaglobulinemia
C17orf62 bd —
C1QB autosomal recessive —
C1QC autosomal recessive —
C1R AD/AR —
C1S autosomal recessive —
C2 autosomal recessive —
C3 AD/AR/MG Complement component 3 deficiency, autosomal recessive, Complement factor B deficiency, Hemolytic uremic syndrome, atypical, susceptibility to, 3
C3AR1 AR/MG Complement factor B deficiency
C4A BG —
C4B autosomal recessive —
C4BPA AD/AR —
C4BPB AD/AR —
C5 AD/AR —
C5AR1 AD/AR —
C5AR2 AD/AR —
C6 autosomal recessive —
C7 autosomal recessive —
C8A AR/MG Complement component 8 deficiency, type I, Complement factor B deficiency
C8B autosomal recessive —
C8G AD/AR —
C9 autosomal recessive Complement component 9 deficiency
CARD11 AD/AR —
CARD14 autosomal dominant —
CARD9 autosomal recessive —
CASP10 autosomal dominant —
CASP8 autosomal recessive Autoimmune lymphoproliferative syndrome, type IIB
CCDC103 autosomal recessive —
CCDC114 autosomal recessive —
CCDC39 autosomal recessive —
CCDC40 autosomal recessive Ciliary dyskinesia, primary, 15
CCDC65 autosomal recessive —
CCNO autosomal recessive —
CD19 autosomal recessive —
CD247 autosomal recessive —
CD27 autosomal recessive —
CD3D autosomal recessive —
CD3E autosomal recessive —
CD3G autosomal recessive —
CD40 autosomal recessive —
CD40LG X-linked —
CD46 AD/AR/MG Complement factor B deficiency, Hemolytic uremic syndrome, atypical, susceptibility to, 3
CD55 BG —
CD59 autosomal recessive —
CD70 — —
CD79A — —
CD79B — —
CD81 — —
CD8A autosomal recessive —
CD93 AD/AR —
CDCA7 — —
CDK9 — —
CEBPE — —
CECR1 autosomal recessive Vasculitis, autoinflammation, immunodeficiency, and hematologic defects syndrome
CFB AD/AR/MG Complement factor B deficiency, Complement factor B deficiency, Hemolytic uremic syndrome, atypical, susceptibility to, 3
CFD autosomal recessive —
CFH AD/AR/MG Complement factor B deficiency, Complement factor H deficiency, Hemolytic uremic syndrome, atypical, susceptibility to, 3
CFHR1 AD/AR/MG Complement factor B deficiency, Hemolytic uremic syndrome, atypical, susceptibility to, 3
CFHR3 AD/AR/MG Complement factor B deficiency, Hemolytic uremic syndrome, atypical, susceptibility to, 3
CFI AD/AR/MG Complement factor B deficiency, Complement factor I deficiency, Hemolytic uremic syndrome, atypical, susceptibility to, 3
CFP X-linked —
CFTR autosomal recessive —
CHD7 autosomal dominant Charge syndrome, Hypogonadotropic hypogonadism 5 with or without anosmia
CIITA autosomal recessive —
CLCN7 AD/AR —
CLPB — —
CLU AD/AR —
COLEC11 autosomal recessive —
COPA — —
CORO1A autosomal recessive —
CR1 AR/MG —
CR2 autosomal recessive —
CRP AD/AR —
CSF2RA X-linked —
CSF2RB — —
CSF3R — —
CTC1 autosomal recessive —
CTLA4 autosomal dominant —
CTPS1 — —
CTSC autosomal recessive —
CXCR4 autosomal dominant Agammaglobulinemia, X-linked, Whim syndrome, Whim syndrome
CYBA autosomal recessive —
CYBB X-linked —
DBR1 — —
DCLRE1C autosomal recessive —
DDX58 autosomal dominant —
DGKE AD/AR/MG Complement factor B deficiency, Hemolytic uremic syndrome, atypical, susceptibility to, 3, Nephrotic syndrome, type 7
DKC1 X-linked —
DNAAF1 autosomal recessive —
DNAAF2 autosomal recessive —
DNAAF3 AD/AR —
DNAH11 autosomal recessive —
DNAH5 autosomal recessive Ciliary dyskinesia, primary, 15
DNAI1 autosomal recessive —
DNAI2 autosomal recessive —
DNAJC21 — —
DNAL1 autosomal recessive —
DNASE2 — —
DNMT3B autosomal recessive —
DOCK2 autosomal recessive —
DOCK8 autosomal recessive Hyper-IgE recurrent infection syndrome
DRC1 AD/AR —
DYX1C1 autosomal recessive —
EFTUD1 bd —
ELANE autosomal dominant Myelodysplastic syndrome, Neutropenia, severe congenital, 1, autosomal dominant
EPG5 — —
ERCC6L2 — —
EXTL3 — —
FADD — —
FAM105B bd —
FAS AD/AR —
FASLG — —
FCHO1 — —
FCN1 AD/AR —
FCN2 AD/AR —
FCN3 autosomal recessive —
FERMT3 autosomal recessive —
FOXN1 — —
FOXP3 X-linked Immunodysregulation, polyendocrinopathy, and enteropathy, X-linked, Immunodysregulation, polyendocrinopathy, and enteropathy, X-linked
G6PC3 autosomal recessive —
G6PD X-linked —
GATA2 autosomal dominant Immunodeficiency 21, Leukemia, acute myeloid, Leukemia, acute myeloid, Myelodysplastic syndrome
GFI1 — —
GINS1 — —
HAX1 autosomal recessive —
HEATR2 bd —
HELLS — —
HYDIN AD/AR —
HYOU1 — —
ICOS — —
IFIH1 autosomal dominant —
IFNAR2 — —
IFNGR1 AD/AR —
IFNGR2 autosomal recessive —
IGHM autosomal recessive —
IGLL1 autosomal recessive —
IKBKG X-linked —
IKZF1 — —
IL10 — —
IL10RA autosomal recessive —
IL10RB autosomal recessive —
IL12B — —
IL12RB1 autosomal recessive —
IL17RA autosomal recessive —
IL17RC — —
IL1RN autosomal recessive —
IL21 — —
IL21R — —
IL23R MG —
IL2RA autosomal recessive —
IL2RB — —
IL2RG X-linked Combined immunodeficiency, X-linked
IL36RN autosomal recessive —
IL6ST — —
IL7 - —
IL7R autosomal recessive Severe combined immunodeficiency, autosomal recessive, T cell-negative, B cell-positive, NK cell-positive
IRAK4 — —
IRF2BP2 — —
IRF8 — —
ISG15 autosomal recessive —
ITGB2 autosomal recessive —
ITK autosomal recessive —
JAGN1 autosomal recessive —
JAK1 - —
JAK3 autosomal recessive Scid, autosomal recessive, T-Negative/b-Positive type
KRAS autosomal dominant Cardiofaciocutaneous syndrome 2
LAMTOR2 — —
LAT — —
LCK autosomal recessive —
LIG1 — —
LIG4 autosomal recessive —
LPIN2 autosomal recessive —
LRBA autosomal recessive —
LRRC6 autosomal recessive —
LYST autosomal recessive Chediak-Higashi syndrome
MAGT1 X-linked Hypomagnesemia 4, renal, Leukemia, acute myeloid
MALT1 autosomal recessive —
MAP3K14 — —
MASP1 autosomal recessive 3MC syndrome 1
MASP2 autosomal recessive —
MAT2A AD/AR —
MEFV AD/AR Familial Mediterranean fever, AR
MKL1 bd —
MOGS autosomal recessive Congenital disorder of glycosylation, type Ii
MRE11A autosomal dominant —
MSN — —
MVK autosomal recessive —
MYD88 — —
MYO5A autosomal recessive Griscelli syndrome, type 1
NBN AD/AR Breast cancer, Nijmegen breakage syndrome
NCF1 autosomal recessive —
NCF2 autosomal recessive —
NCF4 autosomal recessive —
NCSTN — —
NDNL2 bd —
NFKB1 autosomal dominant —
NFKB2 autosomal dominant —
NFKBIA autosomal dominant —
NHEJ1 autosomal recessive Immunodeficiency 124, severe combined, Immunodeficiency 124, severe combined
NHP2 autosomal recessive —
NLRC4 — —
NLRP1 AR/AD —
NLRP12 autosomal dominant —
NLRP3 autosomal dominant Cinca syndrome, Familial cold inflammatory syndrome 1, Muckle-Wells syndrome
NME8 autosomal recessive —
NOD2 MG Blau syndrome, Blau syndrome
NOP10 autosomal recessive —
NRAS autosomal dominant Cardiofaciocutaneous syndrome 2
OFD1 X-linked Joubert syndrome 13, Orofaciodigital syndrome VI, Retinitis pigmentosa, Simpson-Golabi-Behmel syndrome, type 2
ORAI1 autosomal recessive —
PARN AD/AR —
PEPD — —
PGM3 — —
PIGA X-linked Multiple congenital anomalies-hypotonia-seizures syndrome 2
PIK3CD autosomal dominant —
PIK3R1 autosomal recessive Isolated growth hormone deficiency, type III, with agammaglobulinemia
PLCG2 autosomal dominant —
PMS2 AD/AR Diarrhea 5, with tufting enteropathy, congenital
PNP autosomal recessive —
POLD1 autosomal dominant Cardiofaciocutaneous syndrome 2
POLE autosomal dominant Colorectal cancer, susceptibility to, 12
POLE2 — —
POMP — —
PRF1 autosomal recessive —
PRG4 — —
PRKDC autosomal recessive —
PSENEN — —
PSMB8 autosomal recessive —
PSTPIP1 autosomal dominant —
PTPRC autosomal recessive —
PTX3 AD/AR —
RAB27A autosomal recessive Griscelli syndrome, type 1, Griscelli syndrome, type 2
RAC2 - —
RAG1 autosomal recessive Alpha/beta T-cell lymphopenia with gamma/delta T-cell expansion, severe cytomegalovirus infection, and autoimmunity, Alpha/beta T-cell lymphopenia with gamma/delta T-cell expansion, severe cytomegalovirus infection, and autoimmunity, Alpha/beta T-cell lymphopenia with gamma/delta T-cell expansion, severe cytomegalovirus infection, and autoimmunity, Omenn syndrome, Severe combined immunodeficiency, autosomal recessive, T cell-negative, B cell-negative, NK cell-positive
RAG2 autosomal recessive Omenn syndrome, Severe combined immunodeficiency, autosomal recessive, T cell-negative, B cell-negative, NK cell-positive
RASGRP1 — —
RBCK1 autosomal recessive Polyglucosan body myopathy 1 with or without immunodeficiency
RECQL4 autosomal recessive Baller-Gerold syndrome, RAPADILINO syndrome, Rothmund-Thomson syndrome
RELA — —
RFX5 autosomal recessive —
RFXANK autosomal recessive —
RFXAP autosomal recessive —
RHOH AD/AR —
RIPK1 — —
RLTPR bd —
RMRP autosomal recessive Anauxetic dysplasia 1, Cartilage-hair hypoplasia, Metaphyseal dysplasia without hypotrichosis
RNASEH2A autosomal recessive Aicardi-Goutieres syndrome 1
RNASEH2B autosomal recessive Aicardi-Goutieres syndrome 1
RNASEH2C autosomal recessive Aicardi-Goutieres syndrome 1
RNF168 — —
RNF31 — —
RNU4ATAC autosomal recessive —
RORC — —
RPGR X-linked —
RPSA — —
RSPH1 autosomal recessive —
RSPH4A autosomal recessive —
RSPH9 autosomal recessive —
RTEL1 AD/AR —
SAMD9 — —
SAMD9L — —
SAMHD1 autosomal recessive Aicardi-Goutieres syndrome 1
SBDS AD/AR Aplastic anemia, Shwachman-Diamond syndrome 1
SERPING1 AD/AR —
SH2D1A X-linked —
SLC29A3 autosomal recessive —
SLC35C1 autosomal recessive —
SLC37A4 autosomal recessive —
SLC39A7 — —
SLC46A1 autosomal recessive Folate malabsorption, hereditary
SLC7A7 autosomal recessive —
SMARCAL1 autosomal recessive Immunoosseous dysplasia, Schimke type
SMARCD2 — —
SP110 autosomal recessive —
SPAG1 AD/AR —
SPINK5 autosomal recessive Netherton syndrome
SPPL2A — —
SRP54 — —
SRP72 — —
STAT1 AD/AR Immunodeficiency 35
STAT2 autosomal recessive —
STAT3 autosomal dominant Autoimmune disease, multisystem, infantile-onset, 1, Hyper-IgE recurrent infection syndrome
STAT4 AD/AR —
STAT5B autosomal recessive —
STIM1 AD/AR —
STK4 autosomal recessive —
STX11 autosomal recessive —
STXBP2 autosomal recessive —
TAP1 autosomal recessive —
TAP2 autosomal recessive —
TAPBP autosomal recessive —
TBX1 autosomal dominant —
TCF3 — —
TCIRG1 autosomal recessive —
TCN2 autosomal recessive —
TERC autosomal dominant —
TERT AD/AR Aplastic anemia, Pulmonary fibrosis and/or bone marrow failure, telomere-related, 1, Pulmonary fibrosis and/or bone marrow failure, telomere-related, 1
TGFB1 autosomal dominant —
THBD AD/AR/MG Complement factor B deficiency, Hemolytic uremic syndrome, atypical, susceptibility to, 3, Hemolytic uremic syndrome, atypical, susceptibility to, 6
TINF2 autosomal dominant —
TMC6 — —
TMC8 — —
TMEM173 autosomal dominant —
TNFAIP3 — —
TNFRSF13B AD/AR —
TNFRSF1A autosomal dominant —
TNFRSF4 autosomal recessive —
TNFRSF9 — —
TRAC autosomal recessive —
TRAF3IP2 — —
TREX1 AD/AR Aicardi-Goutieres syndrome 1, Vasculopathy, retinal, with cerebral leukodystrophy, Vasculopathy, retinal, with cerebral leukodystrophy
TRNT1 — —
TTC37 autosomal recessive —
TTC7A autosomal recessive —
TYK2 autosomal recessive Immunodeficiency 35
UNC119 autosomal recessive —
UNC13D autosomal recessive —
UNC93B1 — —
UNG — —
USB1 autosomal recessive —
USP18 — —
VPS13B autosomal recessive Cohen syndrome
VPS45 — —
VSIG4 AD/AR —
VTN AD/AR —
WAS X-linked Neutropenia, severe congenital, X-linked, Thrombocytopenia 1, Thrombocytopenia 1
WDR1 — —
WIPF1 — —
WRAP53 autosomal recessive —
XIAP X-linked Lymphoproliferative syndrome, X-linked, 2
ZAP70 autosomal recessive —
ZBTB24 — —
ZMYND10 autosomal recessive —
ZNF341 — —

Click a gene to see a single-gene test.

How the test works

  1. 1

    Order online

    No referral needed. You order online.

  2. 2

    Collect the sample

    Sample: Cheek swab or Venous blood or DNA.

  3. 3

    Result

    Available in 31 days from sample registration in laboratory, online.

Methodology
Methodology
Information on the test method:

At first, deoxyribonucleic acid (DNA) is isolated from a blood sample or paraffin embedded tissue block. The quantity and quality of the material is determined in spectrophotometric and fluorometric assays. From mechanically or enzymatically fragmented DNA a library is made to be used for determination, sequencing and examination of selected genes. The library is sequenced on a new generation sequencer. Afterwards, sequencing results are subjected to bioinformatics analysis and clinical interpretation. Genetic variants are identified using BurrowsWheeler Aligner. The test detects 100% of substitutions and 95% of small insertions and deletions.

Information on variant classification:

The study report provides information on variants classified as ‘potentially pathogenic’ and ‘pathogenic’ depending on their suspected clinical significance. The identified variants are classified under the following categories:

Pathogenic variant: the detected change in the gene sequence directly associates with disease development. At the same time, some pathogenic changes may not have full penetration, meaning that a single mutation may not be enough to cause a full-blown disease.

Potentially pathogenic variant: the detected change in the gene sequence may be, with a great probability, associated with disease development however it is not possible to prove this association on the basis of currently available scientific data. Variant pathogenicity confirmation would require additional tests and evidence; it cannot be excluded that further tests might prove that the change has limited or no clinical significance.

Variant of unknown pathogenicity: based on the currently available scientific data it is not possible to determine the significance of the detected change.

Potentially benign variant: the detected change in the gene sequence most probably does not associate with disease development, however based on the currently available scientific data the benignity of the mutation cannot be confirmed. Confirmation of the clinical significance of the variant would require additional tests and evidence; it cannot be excluded that further tests might prove that the detected mutation has clinical significance and would cause disease development.

Benign variant: the detected change does not associate with disease development.

The identified genetic variants are classified based on the guidelines of the American College of Medical Genetics and Genomics and the American Association for Molecular Pathology (S. Richards, Genet Med. 2015 May; 17(5):405-24). In variant classification the following criteria are considered:

  • Previous variant identification in persons burdened with the disease
  • Variant impact of functional gene product synthesis determined through bioinformatics analyses, confirmed by in vitro/in vivo studies
  • Variant location (exon/intron, functional domain)
  • De novo/hereditary change
  • Variant incidence in general population (each variant with incidence >5% in line with Exome Sequencing Project, 1000 Genomes Project or Exome Aggregation Consortium is classified as benign change)

Variant incidence in general population with relation to patient population The final classification of variants is made on the basis of the total of the above-mentioned criteria. The data bases include: 1000GP, ClinVar, ConsensusPathDB, Exome Aggregation Consortium, Exome Variant Server, FATHMM, GO (Gene Ontology), GTEx (Genotype-Tissue Expression), GWAS (Genome Wide Association Study), HGMD, KEGG, MetaLR, MetaSVM, MutationAssessor, MutationTaster, OMIM, PolyPhen-2, PROVEAN, SIFT, SnpEff, dbNSFP, UniProt, VEP (Variant Effect Predictor).

Test limitations:

All sequencing technologies have some limitations. Our tests use new generation sequencing (NGS) to examine coding and splicing regions of disease-associated genes. Sequencing techniques and subsequent bioinformatics analyses are aimed at limiting the significance of pseudo-gene sequences, however presence of highly homologous gene sequences may still occasionally disturb the identification of pathogenic alleles, deletions/duplications. The Sanger sequencing method is used to confirm variants with lower quality parameters. Deletion/duplication analyses show qualitative changes in DNA covering at least one exon and always require confirmation with other methods (qPCR or MLPA). The analyses are not designed for detecting certain types of genomic changes, such as translocations, inversions, dynamic mutations (e.g. increased number of trinucleotide repetitions) or mutations in regulatory or intronic regions. In case increased numbers of di- or trinucleotide repetitions are reported, it should be assumed that the exact number of repetitions is not precise. The test is not intended to detect somatic mosaicism and somatic mutation analyses should be made in the context of the germinal DNA sequence.

It is not possible to exclude mutations in genes and regions other than those covered by the test as well as alternations in the gene copy number. The test report includes information on changes in gene sequence identified on the basis of a comparison against current reference sequences maintained in NCBI Nucleotide and Ensembl databases. Tests are developed by Warsaw Genomics for clinical objectives. All test results collected are interpreted and analysed by scientific and medical experts of Warsaw Genomics.

Frequently asked questions

How long does the Primary immunodeficiency syndromes test take?

The result is usually available within 31 days from sample registration in laboratory.

Do I need a referral?

No. You can order this genetic test online without a referral.

How many genes does this panel cover?

The panel analyses 354 genes.

How much does the test cost?

The price of the test is 615 EUR.

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