Genetic Analysis of 13 Iranian Families With Leukocyte Adhesion Deficiency Type 1.


Journal

Journal of pediatric hematology/oncology
ISSN: 1536-3678
Titre abrégé: J Pediatr Hematol Oncol
Pays: United States
ID NLM: 9505928

Informations de publication

Date de publication:
01 2019
Historique:
pubmed: 12 5 2018
medline: 15 5 2019
entrez: 12 5 2018
Statut: ppublish

Résumé

Leukocyte adhesion deficiency type 1 is a rare, autosomal recessive disorder that results from mutations in the ITGB2 gene. This gene encodes the CD18 subunit of β2 integrin leukocyte adhesion cell molecules. Leukocyte adhesion deficiency type 1 is characterized by recurrent bacterial infections, impaired wound healing, inadequate pus formation, and delayed separation of the umbilical cord. Blood samples were taken from 13 patients after written consent had been obtained. Genomic DNA was extracted, and ITGB2 exons and exon-intron boundaries were amplified by polymerase chain reaction. The products were examined by Sanger sequencing. In this study, 8 different previously reported mutations (intron7+1G>A, c.715G>A, c.1777 C>T, c.843del C, c.1768T>C, c.1821C>A, Intron7+1G>A, c.1885G>A) and 2 novel mutations (c.1821C>A; p.Tyr607Ter and c.1822C>T; p.Gln608Ter) were found. c.1821C>A (p.Tyr607Ter) and c.1822C>T (p.Gln608Ter) mutations should be included in the panel of carrier detection and prenatal diagnosis.

Sections du résumé

BACKGROUND AND AIM
Leukocyte adhesion deficiency type 1 is a rare, autosomal recessive disorder that results from mutations in the ITGB2 gene. This gene encodes the CD18 subunit of β2 integrin leukocyte adhesion cell molecules. Leukocyte adhesion deficiency type 1 is characterized by recurrent bacterial infections, impaired wound healing, inadequate pus formation, and delayed separation of the umbilical cord.
MATERIALS AND METHODS
Blood samples were taken from 13 patients after written consent had been obtained. Genomic DNA was extracted, and ITGB2 exons and exon-intron boundaries were amplified by polymerase chain reaction. The products were examined by Sanger sequencing.
RESULTS
In this study, 8 different previously reported mutations (intron7+1G>A, c.715G>A, c.1777 C>T, c.843del C, c.1768T>C, c.1821C>A, Intron7+1G>A, c.1885G>A) and 2 novel mutations (c.1821C>A; p.Tyr607Ter and c.1822C>T; p.Gln608Ter) were found.
CONCLUSIONS
c.1821C>A (p.Tyr607Ter) and c.1822C>T (p.Gln608Ter) mutations should be included in the panel of carrier detection and prenatal diagnosis.

Identifiants

pubmed: 29750748
doi: 10.1097/MPH.0000000000001221
doi:

Substances chimiques

CD18 Antigens 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e3-e6

Auteurs

Shahram Teimourian (S)

Department of Medical Genetics.
Department of Infectious Diseases, Pediatric Infectious Diseases Research Center, School of Medicine.

Martin De Boer (M)

Sanquin Research, and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

Dirk Roos (D)

Sanquin Research, and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

Anna Isaian (A)

Department of Pathology, Tehran University of Medical Sciences (TUMS), Tehran, Iran.

Mohammad Hassan Bemanian (MH)

Department of Allergy and Clinical Immunology, Hazrat Rasool Hospital.

Sharhzad Lashkary (S)

Department of Medical Genetics.

Mohammad Nabavi (M)

Department of Allergy and Clinical Immunology, Hazrat Rasool Hospital.

Saba Arshi (S)

Department of Allergy and Clinical Immunology, Hazrat Rasool Hospital.

Alireza Nateghian (A)

Department of Pediatrics, Ali Asghar Children Hospital.

Shirin Sayyahfar (S)

Department of Pediatrics, Ali Asghar Children Hospital.

Faezeh Sazgara (F)

Department of Medical Genetics.

Gholamreza Taheripak (G)

Department of Biochemistry.

Elham Alipour Fayez (E)

Department of Immunology, School of Medicine, Iran University of Medical Sciences (IUMS).

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