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Our comprehensive 97-gene immunogenetic testing panel is designed to analyze the key genes that govern immune regulation, inflammation, antigen presentation, and immunomodulated treatment response. This test provides clinical professionals with deeper insight into how immune genetics influence individual patient outcomes, paving the way for safer, more effective, and personalized medical care.
This test is ideal for patients with:
Cancer: When immune checkpoint inhibitors or other immunotherapies are being considered.
Autoimmune disorders: Such as lupus, rheumatoid arthritis, multiple sclerosis, or inflammatory bowel disease.
Chronic inflammatory diseases: Including asthma, psoriasis, or chronic fatigue syndrome.
Immunodeficiency or hyperreactivity: Where the immune response appears atypical or unpredictable.
Recurrent infections: Suggesting a possible immune dysfunction.
Adverse drug reactions: Particularly those related to immunotherapy, biologic agents, or vaccines.
Family history of immune or inflammatory disease.
Our selected panel focuses on scientifically validated or emerging clinically significant genes involved in immune regulation. The categories include:
Immune checkpoint pathways:
PD-1, PD-L1, CTLA-4, LAG3, TIM3 — regulate T-cell activation and immune surveillance
Cytokine and chemokine signaling:
IL2, IL6, IL10, TNF-alpha, IFN-gamma — mediate inflammation, immune suppression, and resolution
Antigen processing and HLA typing:
Genes involved in antigen presentation and immunodominance (HLA-A, HLA-B, HLA-C, HLA-DR)
T-cell and B-cell signaling:
Key components in adaptive immune activation and tolerance
Tumor intrinsic immune escape:
Genes that modulate the ability of cancer cells to evade immune detection
Immunogenetic risk markers:
Associated with susceptibility to autoimmune and inflammatory diseases
Genes analyzed: 97 selected immunogenetic targets
Technology platform: High-throughput next-generation sequencing (NGS)
Coverage depth: >98% at >20x depth across specific exons and intronic boundaries
Bioinformatics process: Clinically validated with high analytical accuracy; data interpreted according to AMP/ACMG guidelines
Complementary testing: Sanger confirmation or additional assays performed when necessary
Turnaround time: 10 calendar days
Oncology and Immunotherapy Optimization
Identify patients most likely to respond to checkpoint inhibitors and other immunologic therapies.
Stratify patients based on immune tolerance and toxicity risk.
Inform combination strategies with targeted therapy or chemotherapy.
Predict secondary resistance or the need for rechallenge in cases of relapse.
Autoimmune and Chronic Inflammatory Disorders
Detect genetic predispositions to autoimmunity.
Guide therapeutic choices among immunosuppressants, biologic agents, and lifestyle interventions.
Educate families on screening and risk prevention strategies.
Infectious Diseases and Vaccine Response
Understand patient variability in pathogen susceptibility and vaccine efficacy.
Assess immune system resilience or the potential for hyperactivation.
Personalize booster or biologic therapy regimens.
General Immune Wellness
Monitor immunogenetic profiles in complex cases with unexplained symptoms.
Provide early warning of systemic inflammation, immune dysregulation, or rare immunologic disorders.
Support long-term care planning for chronic or recurrent conditions.
This immunogenetic panel is best used as part of a multidimensional diagnostic strategy, often in combination with:
Somatic tumor testing (e.g., NGS solid tumor profiling)
Pharmacogenetic testing (for drug metabolism and gene–drug interactions)
Germline genetic testing (for hereditary disease risk and preventive care planning)
Together, these tools enable precision medicine teams to deliver a fully personalized, data-driven treatment plan for each patient.
Immunogenetic testing is no longer limited to oncology. It is a fundamental pillar of modern precision medicine, helping clinicians understand the role of the immune system across a wide spectrum of diseases. With a robust 97-gene panel, rapid turnaround, and evidence-based reports, Genuvi enables professionals to provide safer, smarter, and more personalized care—one immune gene at a time.
Test Methodology:
The Comprehensive Immunology Panel is designed to detect single nucleotide variants (SNVs) and small insertions and deletions in 96 genes associated with the risk of immunologic disorders. The target regions include coding exons and the 10 bp intronic sequences immediately adjacent to each exon–intron boundary of every coding exon. Patient DNA is prepared using targeted hybrid capture, assigned a unique index, and sequenced using Illumina sequencing-by-synthesis (SBS) technology. Data are aligned to the human genome build GRCh37. Variant interpretation follows the current professional guidelines of the American College of Medical Genetics and Genomics (ACMG) using FabricEnterprise™ Pipeline 6.6.15. Interpretation and reporting are performed by Fabric Clinical (CLIA ID: 45D2281059, CAP ID: 9619501), located at 6901 Quaker Avenue, Suite A, Lubbock, Texas, 79413. Quality filters applied to all variants include: quality <500, allelic balance <0.3, coverage <10x.
Genes Analyzed:
ADA, AIRE, ARX, ATM, ATRX, BLM, BRCA1, BRCA2, BTK, C1QBP, CASP10, CD40, CD70, CDKL5, CEBPA, CFTR, CHD7, COPA, CR2, CTLA4, CYBA, CYBB, DNASE2, EPCAM, F13B, F5, F7, F9, FANCC, FAS, FASLG, FCHO1, FGB, FGD1, FMR1, FOXP3, G6PC, G6PD, GP1BB, HUWE1, HYOU1, IL1RAPL1, IL23R, IL2RB, IL2RG, IL6R, IL6ST, IL7R, ITCH, JAK1, JAK2, JAK3, KDM5C, KRAS, L1CAM, LIG1, LIG4, LRBA, MAP3K14, MECP2, MED12, MEFV, MID1, MKL1, MLH1, MPL, MSH2, MSH6, MTHFD1, MYD88, NF1, NFKB1, NFKB2, NHEJ1, NRAS, OCRL, PALB2, PLCG2, PMS2, POLE2, PRKCD, PTEN, PTPRC, RASGRP1, RELA, RIPK1, RLTPR, RPS6KA3, RUNX1, SLC16A2, SPPL2A, STAT3, TERT, TNFRSF13B, TP53, VPS13B
Test Limitations:
This test is intended to detect all clinically relevant variants within the coding regions of the evaluated genes. Pathogenic and likely pathogenic variants must be confirmed by orthogonal methods. Variants classified as benign, likely benign, or of uncertain significance (VUS) are not reported.
Homopolymeric regions and sequences outside coding regions cannot be captured using standard NGS target enrichment protocols. The assay does not detect large deletions or duplications, nor variants in unanalyzed regions (e.g., introns, promoters, enhancers, long repeats, mitochondrial sequences). It is not designed to detect mosaicism, complex genetic rearrangements, or genomic aneuploidy events.
Variants may exist in these genes that are undetectable with current technology, and some genes may have uncertain clinical relevance. Thus, the test may not detect all variants associated with immunologic pathology. Variant interpretation is based on current knowledge and ACMG guidelines, which may change over time.
Factors affecting DNA quantity and quality include collection technique, amount of buccal epithelial cells, oral hygiene, dietary or microbial nucleic acids, and other interfering substances. PCR inhibitors, foreign DNA, and nuclease activity may negatively impact assay performance.
Regulatory Disclosures
This laboratory-developed test (LDT) was designed and its performance characteristics were determined by Genuvi. The test was performed at Genuvi, a laboratory certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA) as qualified to perform high-complexity testing.
This assay has not been cleared or approved by the U.S. Food and Drug Administration (FDA). FDA clearance or approval is not required for the clinical use of this analytically and clinically validated laboratory test. This assay has been developed for clinical purposes only and should not be considered for research use.
References:
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Beutler E, Kuhl W, Vives-Corrons JL, Prchal JT. Blood. November 15, 1989. Molecular heterogeneity of glucose-6-phosphate dehydrogenase A. (PMID: 2572288)
Hirono A, Beutler E. Proceedings of the National Academy of Sciences of the United States of America. June 1988. Molecular cloning and nucleotide sequencing of cDNA for the A(-) variant of human glucose-6-phosphate dehydrogenase. (PMID: 2836867)
Yoshida A, Stamatoyannopoulos G, Motulsky AG. Science (New York, NY). January 6, 1967. The Negro variant of human glucose-6-phosphate dehydrogenase deficiency (A-). (PMID: 6015571)
Gómez-Gallego F, Garrido-Pertierra A, Bautista JM. Journal of Biological Chemistry. March 31, 2000. Structural defects underlying protein dysfunction in human glucose-6-phosphate dehydrogenase deficiency A(-). (PMID: 10734064)
Hirono A, Kawate K, Honda A, Fujii H, et al. Blood. February 15, 2002. A single 202G>A mutation in the human glucose-6-phosphate dehydrogenase gene (G6PD) can cause acute hemolysis on its own. (PMID: 11852882)
Dallol A, Banni H, Gari MA, Al-Qahtani MH, et al. Journal of Translational Medicine. September 24, 2012. Five new haplotypes of glucose-6-phosphate dehydrogenase deficiency correlate with disease severity. (PMID: 23006493)
Shah SS, Macharia A, Makale J, Uyoga S, et al. BMC Medical Genetics. September 9, 2014. Genetic determinants of glucose-6-phosphate dehydrogenase activity in Kenya. (PMID: 25201310)
