Medical Policy

This document addresses gene therapy for severe leukocyte adhesion deficiency type I (LAD-I), a rare, inherited, immunodeficiency disorder caused by a mutation in the ITGB2 gene, which causes leukocytes to be unable to migrate to the site of infection to kill offending microbes. Individuals with LAD-I exhibit earlier, more frequent, and more serious episodes of infection than individuals who do not have this disorder. These infections often lead to death before the age of 2 years if hematopoietic stem cell transplantation (HSCT) is not performed.

One gene therapy is approved by the Food and Drug Administration (FDA) to treat LAD-I: marnetegragene autotemcel (KRESLADI^™). Marnetegragene autotemcel is an infusion of autologous CD34+ hematopoietic stem and progenitor cells transduced by a self-inactivating lentiviral vector encoding for the ITGB2 gene.

Note: For additional information regarding other disease modifying treatments for LAD-I, please see:

• TRANS.00029 Hematopoietic Stem Cell Transplantation for Genetic Diseases and Aplastic Anemias

Note: For a high-level overview of this document, please see “Summary for Members and Families” below.

Medically Necessary:

A one-time infusion of marnetegragene autotemcel is considered medically necessary in individuals when all of the following criteria (A through D below) are met:

1. Confirmed diagnosis of severe leukocyte adhesion deficiency-I (LAD-I) has been made (either criterion 1 or 2 below must be met):
   1. Flow cytometry indicating CD18 expression on less than 2% neutrophils (polymorphonuclear neutrophils [PMNs]) when the following criterion is met:
      1. Clinical history consistent with severe leukocyte adhesion deficiency-I (LAD-I) phenotype^a
         or
   2. Flow cytometry indicating CD18 expression on more than 2% PMNs when all of the following criteria are met (a through c):
      1. Less than 2% CD11a or CD11b expressing PMNs; and
      2. Documented ITGB2 mutation; and
      3. Either of the following:
         1. Clinical history consistent with severe leukocyte adhesion deficiency-I (LAD-I) phenotype^a; or
         2. Documented family history of LAD-I;
            and
2. The individual is a candidate for an allogeneic hematopoietic cell transplantation, but ineligible due to the absence of a donor^b; and
3. No serious concomitant illness is present (for example, severe hepatic dysfunction, severe renal dysfunction, severe pulmonary dysfunction, active metastatic or advanced malignancy, active serious infection, or significant medical conditions, including documented human immunodeficiency virus (HIV) or congestive heart failure).

^a Refer to the Rationale section for information on severe leukocyte adhesion deficiency-I (LAD-I) phenotype.
^b Documentation that a suitable donor has not been identified.

Investigational and Not Medically Necessary:

Gene therapy for severe leukocyte adhesion deficiency-I (LAD-I) is considered investigational and not medically necessary when the criteria above are not met, and in all other situations.

This document describes clinical studies and expert recommendations, and explains whether gene therapy for severe leukocyte adhesion deficiency type I (LAD-I) is clinically appropriate. The following summary does not replace the medical necessity criteria or other information in this document. The summary may not contain all of the relevant criteria or information. This summary is not medical advice. Please check with your healthcare provider for any advice about your health.

Key Information

LAD-I is a rare genetic condition where the body’s white blood cells cannot move to fight infections. This is because of a missing or faulty gene called ITGB2. People with this condition often have repeated, serious infections from a young age, and many do not live past the age of 2 without treatment. The usual treatment for LAD-I is a stem cell transplant. However, that treatment is not available to everyone due to the need for a well matched stem cell donor. Marnetegragene autotemcel (Kresladi) is a gene therapy that may help people with LAD-I who cannot get a stem cell transplant. This gene therapy uses the person’s own stem cells, which are changed in a lab to add a healthy copy of the ITGB2 gene. These cells are then returned to the person in a one-time infusion. This may help white blood cells work correctly and fight infection.

What the Studies Show

LAD-I is caused by a change in the ITGB2 gene, which leads to very low levels of a protein called CD18. Without this protein, white blood cells cannot reach infection sites, leading to frequent and serious infections starting in infancy. Without treatment, many children do not survive past age 2. Before gene therapy, the only curative option was a donor stem cell transplant, which can be limited by donor availability and may cause serious complications.

In a small study of 9 children, all treated with this gene therapy were alive after at least 1 year and did not need a donor transplant. Children treated before age 1 were also alive after age 2. The treatment helped restore immune function, reduce infections, and lower hospital stays. No serious side effects were directly linked to the gene therapy itself, but some side effects occurred from the chemotherapy given before treatment, including low blood counts and inflammation. Two children had serious health events related to treatment procedures, but these were resolved with care. Because this was a small study, larger studies are needed to confirm long-term safety and benefits.

When is Marnetegragene Autotemcel (Kresladi) Clinically Appropriate?

Marnetegragene autotemcel (Kresladi) may be appropriate in these situations:

• The person has a confirmed diagnosis of severe LAD-I based on lab testing and a history of serious infections; and
• The person could receive a donor stem cell transplant but does not have a suitable donor; and
• The person does not have serious other health conditions, such as severe liver, kidney, or lung disease, active cancer, or severe infection.

When is this not Clinically Appropriate?

This treatment is not clinically appropriate when the criteria above are not met. This is because studies have only shown benefit in people who meet these specific conditions. Using it in other situations has not been proven to improve health. Unnecessary or unproven treatments can lead to needless worry, or to treatment that does not help. Marnetegragene autotemcel (Kresladi) is not clinically appropriate in scenarios other than those listed above.

(Return to Description/Scope)

Summary

Leukocyte adhesion deficiency type I (LAD-I) is a very rare genetic disorder affecting about one in 1 million people. It is caused by mutations in the ITGB2 gene that makes CD18, a protein that helps white blood cells reach infection sites. Without CD18, affected individuals face recurrent, life-threatening infections and rarely survive past childhood without treatment.

Kresladi (marnetegragene autotemcel, developed by Rocket Pharmaceuticals) is the first FDA-approved gene replacement therapy (approved March 2026) to treat pediatric patients with severe leukocyte adhesion deficiency-I (LAD-I) due to biallelic variants in ITGB2 who do not have an available human leukocyte antigen (HLA)-matched sibling donor for allogeneic HSCT. It performs as a corrective, patient-derived stem cell therapy designed to restore immune function and reduce fatal infections. Kresladi is administered as a one-time intravenous infusion.

Based on the 2-year study results of a phase 1/2 multinational trial, participants treated with Kresladi demonstrated significant improvements in survival and all participants survived without undergoing HSCT and remained free of disease symptoms, including skin lesions and severely inflamed gums. All 3 participants who were enrolled younger than 1 year of age were alive after 2 years of age. The gene therapy achieved lasting immune system restoration, characterized by neutrophil CD18 expression rising above 10% of normal levels in all participants. Furthermore, there was a 74% reduction in hospitalizations related to infections. The study result suggest that the marnetegragene autotemcel gene therapy may provide lifechanging and durable benefits for individuals with LAD-I.

Discussion

Leukocyte adhesion deficiency (LAD) is a rare, autosomal recessive immunodeficiency disease caused by recessive pathogenic mutations in the ITGB2 gene, which results in impaired surface expression of CD18. The leukocytes, particularly the neutrophils, are unable to adhere to the endothelial cell wall and migrate to the site of infection. The severity of infectious complications appears to be directly related to the degree of defective CD18 expression.

Two phenotypes for LAD, moderate deficiency and severe deficiency, have been identified.

• Moderate Deficiency Phenotype
  Individuals with the mild-moderate deficiency phenotype have approximately 2-30% percent of normal CD18 expression and experience fewer serious infectious episodes and typically survive into adulthood. Treatment of infections in individuals with moderate deficiency usually respond to supportive care and antibiotic therapy.
• Severe Deficiency Phenotype
  Individuals with the more severe form of the disease (LAD-I), have < 2% of the normal surface CD18 expression and experience earlier, more frequent, and more serious episodes of bacterial and fungal infections. Infections affecting the skin, respiratory tract, bowel, and perirectal areas are generally apparent from birth onward. Clinical manifestations of LAD-I include delayed separation of the umbilical cord, recurrent bacterial infections, especially of the mucosal surfaces and skin, absent pus formation, leukocytosis, impaired wound healing and later in life, periodontitis. If untreated, LAD-I often results in death prior to the age of 2 years.

Prior to gene therapy for LAD-I, HSCT was the only curative treatment for the disease. While allogeneic HSCT is potentially curative, it is limited by donor availability, graft-versus-host disease, and graft failure. Researchers have explored the use of lentiviral vectors to insert a functional copy of the ITGB2 gene to restore CD18 surface expression.

Booth and colleagues (2022) reported the results of clinical trial NCT03812263 in which gene therapy RP-L201-0318 utilized autologous CD34+ cells transduced with a lentiviral vector carrying ITGB2 to restore CD18 expression in infants with severe LAD-I. All study participants were at least 3 months of age. HSCs were collected via apheresis post mobilization with granulocyte-colony stimulating factor and plerixafor and transduced ex-vivo with Chim-CD18-WPRE-LV. Myeloablative therapeutic drug monitoring (TDM) busulfan conditioning was done prior to the RP-L201 infusion. Participants were followed for safety and efficacy measures, including survival to age 2 and ≥ 1-year post-infusion, peripheral blood [PB] PMN CD18 expression, PB vector copy number [VCN], neutrophilia improvement, decrease in hospitalizations/infections, and resolution of periodontal/skin abnormalities.

A total of 9 participants, ranging in age from 5 months to 9 years, received RP-L201. Follow-up was carried out at 3 and 24 months. RP-L201 cell doses varied between 2.8 × 10⁶ to 10.0 × 10⁶ CD34+ cells/kg with a drug product VCN of 1.8 to 3.8. All 9 participants demonstrated PMN CD18 restoration (median expression of 56.3%) with sustained, stable genetic markings (median PB mononuclear cell VCN of 1.53). At 1 year, the overall survival (OS) rate amongst the participants was 100% per Kaplan-Meier estimate. Pre-treatment leukocytosis improved consistently. Hospitalizations and severe infections significantly declined following gene therapy. No serious RP-L201-related adverse events (SAEs) were reported. Insertion site analyses indicate highly polyclonal integration patterns across the entire group. The researchers reported a favorable safety profile and concluded RP-L201confers durable correction of the severe LAD-I phenotype and, as demonstrated by all laboratory and clinical parameters, resulted in an improved clinical course in all 9 pediatric participants. These findings were presented in abstract form by the American Society of Hematology (ASH) and have not yet been published in the peer-reviewed literature.

In May 2023, the 3-34 month follow-up data was published in abstract form only (Booth 2023). The authors reported:

All nine participants demonstrated PMN CD18 restoration (median expression of 56.3%) with sustained, stable genetic markings (median PB mononuclear cell VCN of 1.53). At one year, the overall survival (OS) rate was 100% per Kaplan-Meier estimate. Pre-treatment leukocytosis improved uniformly. Hospitalizations and severe infections were significantly reduced following therapy. No RP-L201-related serious adverse events (SAEs) were reported. Insertion site analyses indicate highly polyclonal integration patterns across the entire cohort.

Booth and colleagues (2025) reported the results of the continuation of a Phase 1/2 clinical trial evaluating the safety and efficacy of RP-L201 2 years post infusion. A total of 9 participants with severe LAD-1, aged 5 months to 9 years, were treated with RP-l201 and followed for 24 months. The primary efficacy endpoint of the phase 2 study was to determine if children could survive without needing an allogeneic HSCT at least 1 year after RP-L201 infusion and at 2 years of age among the participants who were younger than 1 year of age at enrollment. Study outcomes were compared to an expected survival rate of 39%.

With regard to safety, the most common adverse events that occurred during treatment included anemia in all 9 participants, mucosal inflammation in 7 participants (78%), all of which were attributed to myeloablative busulfan conditioning. A total of 6 participants (67%) experienced decreased platelet count. Two participants experienced 3 serious adverse events: 1 participant developed grade 3 hepatic veno-occlusive disease and grade 4 pulmonary arterial hypertension, both of which resolved with treatment. Another participant experienced a grade 3 deep vein thrombosis related to the placement of a central intravenous catheter, which was resolved without complications. All of the serious adverse events were determined by the investigator to be caused by either preinfusion treatments, study procedures, or both, including conditioning therapy. No adverse events ascribed to gene therapy were reported. None of the patients had graft failure.

With regard to the primary end point, HSCT-free survival was 100% (95% confidence interval [CI], 66 to 100) at 1 year after infusion (p<0.001). All the participants who were enrolled at younger than 1 year of age were alive beyond 2 years of age. In contrast, historical data demonstrate that 39% of children with severe LAD-I who do not undergo allogeneic HSCT are alive beyond the age of 2 years (p<0.001). Additionally, all the participants were alive at least 1.8 years after RP-L201 (range, 1.8 to 3.73); none of the participants underwent allogeneic HSCT during the cumulative follow-up of 22.37 patient-years. All 3 participants who were enrolled during early infancy (≤ 1 year of age) were alive beyond 2 years of age without undergoing allogeneic HSCT (100% HSCT-free survival). Event free survival (no graft failure or graft versus host disease [GVHD]) amongst participants was 100%.

The study results also demonstrated a markedly lower annualized incidence of prespecified serious infections, infection-related hospitalizations, and prolonged infection-related hospitalizations following treatment than before treatment with RP-L201. In addition, LAD-I-related skin lesions resolved, and participants demonstrated normal wound healing after gene therapy. The annualized incidence of infection-related hospitalizations beyond 90 days post engraftment through 24 months after RP-L201 infusion was 74.45% lower than the incidence before RP-L201, the annualized incidence of prespecified serious infections was 84.90% lower and the annualized incidence of prolonged infection-related hospitalizations was 81.95% lower. Pretreatment neutrophilia related to LAD-I also resolved.

The researchers reported no evidence of replication-competent lentivirus, oligoclonality, or insertional mutagenesis was found. Additionally, seven participants discontinued supportive care measures such as antimicrobial prophylaxis and the study results demonstrated no increased susceptibility to infections after discontinuation.

The researchers concluded that RP-L201 corrected the genetic defect underlying LAD-I and resulted in a sustained phenotypic reversal of severe LAD. A limitation of the study is its small sample size which is due to the rarity of LAD-I in the general population.

Study eligibility criteria listed in clinicaltrials.gov for NCT03812263 are as follows (Rocket Pharmaceuticals Inc., 2023):

Inclusion Criteria

• A confirmed diagnosis of severe LAD-I as demonstrated by flow cytometry indicating CD18 expression on <2% neutrophils (polymorphonuclear neutrophils (PMNs)). Subjects in which CD18+ PMNs are >2% will be considered eligible with <2% CD11a or CD11b expressing PMNs and if there is a documented ITGB2 mutation and clinical history consistent with LAD-I (or known family history).
• At least one (1) prior significant bacterial or fungal infection US NCI CTCAE, v5.0, Grade ≥2). This criterion is not required for subjects with documented family history who meet the above inclusion criteria.
• Age ≥3 months.
• Considered to be an appropriate candidate for autologous transplantation of hematopoietic stem cells.
• A competent custodial parent with legal capacity to execute an institutional review board (IRB)/ethics committee (EC)-approved consent form must be available to participate in the consent process. (Informed assent will be sought from capable subjects, in accordance with the directive of the IRB/EC and with local requirements).
• Ability to comply with trial procedures including investigational therapy and follow-up evaluations.

Exclusion Criteria

• Availability of a medically-eligible human leukocyte antigen (HLA)-identical sibling donor transplant. Subjects may not be included in this trial as an alternative to a clinically-indicated and feasible HLA-matched sibling donor hematopoietic stem cell transplant. If an HLA-identical sibling is identified, but mobilized peripheral blood or bone marrow hematopoietic stem cell collection is not feasible (for example: donor is in utero, is a newborn from whom cord blood was not collected, or is unable to undergo donation procedure because of medical impairments), then inclusion may be permitted per Investigator discretion.
• Hepatic dysfunction as defined by either:
  • Bilirubin >1.5× the upper limit of normal (ULN) or
  • Alanine aminotransferase (ALT) or aspartate aminotransferase (AST) >2.5×ULN.
• Renal dysfunction as defined by either Grade 3 or higher abnormalities in serum sodium, potassium, calcium, magnesium or phosphate as defined by NCI CTCAE v5.0, or the requirement for either peritoneal dialysis or hemodialysis.
• Pulmonary dysfunction as defined by either:
  • Need for supplemental oxygen during the prior 2 weeks (in absence of acute infection).
  • Oxygen saturation (by pulse oximetry) <90%.
• Evidence of active metastatic or locoregionally advanced malignancy (including hematologic malignancy) for which survival is anticipated to be less than 3 years.
• Serious infections with persistent bloodstream pathogens at time of trial entry. (Subjects with active infections (e.g., unresolved ulcerative lesions, skin or oral infections) are permitted as long as appropriate antibiotic therapy has been (or is being) administered).
• Any medical or other contraindication for both leukapheresis and bone marrow harvest procedure, as determined by the treating Investigator.
• Any medical or other contraindication for the administration of conditioning therapy, as determined by the treating Investigator.
• Significant medical conditions, including documented human immunodeficiency virus (HIV) infection, poorly-controlled diabetes, poorly-controlled hypertension, poorly-controlled cardiac arrhythmia or congestive heart failure; or arterial thromboembolic events (including stroke or myocardial infarction) within the 6 prior months.
• Any medical or psychiatric condition that in the opinion of the Investigator renders the subject unfit for trial participation or at higher than acceptable risk for participation.

Based on the existing body of evidence, the use of marnetegragene autotemcel gene therapy may be a reasonable treatment option for individuals of any age with severe LAD-1, bypassing the three-month minimum age restriction in the pivotal trial (NCT03812263). Due to the high mortality rate of severe LAD-1 in early childhood, gene therapy may be considered appropriate for individuals with severe LAD-I who are candidates for allogeneic hematopoietic cell transplantation but lack an available donor, provided they do not have a serious concurrent illness.

LAD-I is a rare, inherited combined deficiency disorder of the immune system which has been estimated to affect 1 in 1 million people annually. The disorder typically presents shortly after birth with recurrent, indolent bacterial infections. LAD-I is characterized by an inability of leukocytes to migrate to the site of infection to kill offending microbes (StatPearls, 2023).

Historically, HSCT has been the only curative treatment for LAD-I, but the procedure is limited by graft-versus-host disease and related toxicities. At least one trial in combination with busulfan conditioning, explored the use of lentiviral vectors to insert a functional copy of the ITGB2 gene to restore CD18 surface expression (Booth, 2022).

Common Terminology Criteria for Adverse Events (CTCAE)

The Common Terminology Criteria for Adverse Events (CTCAE) are a set of criteria developed by the United States National Cancer Institute (NCI) for the standardized classification of adverse effects of oncologic therapies. According to the CTCAE (V6), an adverse event is defined as follows:

An Adverse Event (AE) is any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with the use of a medical treatment or procedure that may or may not be considered related to the medical treatment or procedure. An AE is a term that is a unique representation of a specific event used for medical documentation and scientific analyses.

The most current version (6.0) was published in September 2025. The use of the CTCAE classification system has expanded so that now, many clinical trials, including those that are not oncology related, document their observations based on the CTCAE system.

The CTCAE uses grades (1-5) and a clinical description to define the severity of an adverse event. The general grading system is provided below.

Grade 1           Mild; asymptomatic or mild symptoms; clinical or diagnostic observations only; intervention not indicated.
Grade 2           Moderate; minimal, local or noninvasive intervention indicated; limiting age-appropriate instrumental ADL*.
Grade 3           Severe or medically significant but not immediately life-threatening; hospitalization or prolongation of hospitalization indicated; disabling; limiting self-care ADL**.
Grade 4           Life-threatening consequences; urgent intervention indicated.
Grade 5           Death related.

*                      Instrumental ADL refer to preparing meals, shopping for groceries or clothes, using the telephone, managing money, etc.
**                    Self-care ADL refer to bathing, dressing and undressing, feeding self, using the toilet, taking medications, and not bedridden.

More detailed information about the CTCAE criteria can be found at: US NCI CTCAE.

Allogeneic: Tissue or cells taken from different individuals from the same species.

Autosomal recessive disease: An inherited condition for which two copies of an abnormal gene must be present for the condition or trait to develop.

Conditioning: A preparative regimen of chemotherapy given as part of a bone marrow/peripheral blood stem cell transplant protocol.

Ex vivo: Outside of the living body. Ex vivo gene therapy refers to the process of taking an organ, cells, or tissue from a living body for a treatment or procedure, and then returning the organ, cells, or tissue to the living body.

Gene replacement therapy: A medical treatment that introduces or alters genetic material to replace the function of a missing or dysfunctional gene with the goal of lessening or eliminating a disease process that results from genetic dysfunction; also known as gene therapy.

Graft-versus-host disease (GVHD): The condition that results when the immune cells of a transplant (usually of bone marrow) react against the tissues of the person receiving the transplant.

Hematopoietic stem cells: Cells that give rise to distinct daughter cells, one cell that replicates the stem cell and one cell that will further proliferate and differentiate into a mature blood cell; also called progenitor cells.

Lentiviral vector: A type of virus that is used as a vehicle for gene delivery. Lentiviral vectors are derived from Human immunodeficiency virus type-1 (HIV-1) lentivirus but are unable to replicate and hence are considered relatively safe.

The following codes for treatments and procedures applicable to this document are included below for informational purposes. Inclusion or exclusion of a procedure, diagnosis or device code(s) does not constitute or imply member coverage or provider reimbursement policy. Please refer to the member's contract benefits in effect at the time of service to determine coverage or non-coverage of these services as it applies to an individual member.

When services may be Medically Necessary when criteria are met:

When services are Investigational and Not Medically Necessary:
For the procedure and diagnosis codes listed above when criteria are not met or for all other diagnoses not listed.

Peer Reviewed Publications:

1. Booth C, Sevilla J, Almarza E, et al. Lentiviral gene therapy for severe leukocyte adhesion deficiency type 1. N Engl J Med. 2025; 392(17):1698-1709.
2. Booth C, Sevillia J, Chitty Lopex, M, et al. Severe leukocyte adhesion deficiency-I (LAD-I) lentiviral mediated ex-vivio gene therapy: ongoing phase1/2 study results. Clin Immunol. 2023; 250(suppl): 10954. Abstract.
3. Booth C, Sevilla J, Rao GR, et al. Interim results from an ongoing phase 1/2 study of lentiviral-mediated ex-vivo gene therapy for pediatric patients with severe leukocyte adhesion deficiency-I (LAD-I). Blood 2022; 140:7774-7775. Abstract.
4. Harris ES, Weyrich AS, Zimmerman GA. Lessons from rare maladies: leukocyte adhesion deficiency syndromes. Curr Opin Hematol. 2013; 20(1):16-25.
5. Heimall J, González-Granado LI, Booth C, et al. International clinical consensus on leukocyte adhesion deficiency-I: modified Delphi analysis. J Allergy Clin Immunol Glob. 2026;5(3):100682.

Government Agency, Medical Society, and Other Authoritative Publications:

1. Common Terminology Criteria for Adverse Events (CTCAE), V6.0. Revised September 29, 2025. National Institutes of Health, National Cancer Institute (NCI). Available at: https://dctd.cancer.gov/research/ctep-trials/for-sites/adverse-events#ctcae. Accessed on April 2, 2026.
2. Justiz Vaillant AA, Ahmad F. Leukocyte adhesion deficiency. [Updated July 3, 2023]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023. Available at: https://www.ncbi.nlm.nih.gov/books/NBK539770/. Accessed on April 2, 2026.
3. United States Food and Drug Administration (FDA). Rockville, MD: FDA. Kresladi (marmetegragene autotemcel suspension for intravenous infusion. Initial U.S. Approval: March 2026. Available at: https://www.fda.gov/media/191722/download?attachment. Accessed on April 2, 2026.
4. U.S. National Library of Medicine. Clinicaltrials.gov. A clinical trial to evaluate the safety and efficacy of RP-L201 in subjects with leukocyte adhesion deficiency-I. NCT03812263. Last Updated November 15, 2023. Available at: https://clinicaltrials.gov/study/NCT03812263?intr=RP-L201&rank=1. Accessed on April 2, 2026.

1. National Organization for Rare Disorders (NORD). Leukocyte adhesion deficiency type I. https://rarediseases.org/mondo-disease/leukocyte-adhesion-deficiency-1/. Accessed on February 3, 2026.
2. National Organization for Rare Disorders. Information Center. Leukocyte Adhesion Deficiency Syndromes. Last updated March 14, 2018. Available at: https://rarediseases.org/rare-diseases/leukocyte-adhesion-deficiency-syndromes/. Accessed on April 2, 2026.

Leukocyte adhesion deficiency-I (LAD-I)
Marnetegragene autotemcel

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