Chronic granulomatous disease (CGD) is a primary immunodeficiency disorder characterized by defective microbial killing in phagocytes. Long-term prognosis for CGD patients is generally poor, highlighting the need to develop minimally toxic, curative therapeutic approaches. We here describe the establishment of a mouse model in which X-linked CGD can be cured by allogeneic bone marrow transplantation. Using a combination of non-myeloablative-dose total body irradiation and a single injection of anti-CD40 ligand monoclonal antibody, transplantation of whole bone marrow cells achieved long-lasting mixed chimerism in X-linked CGD mice in a haploidentical transplantation setting. Stable mixed chimerism was maintained for up to 1 year even at a low range (<20 % donor cells), indicating induction of donor-specific tolerance. The regimen induced mild myelosuppression without severe acute complications. Stable chimerism was therapeutic, as it suppressed cutaneous granuloma formation in an in vivo test suited for evaluation of treatment efficacy in murine CGD models. These results warrant future development of a simplified allogeneic hematopoietic cell transplantation regimen that would benefit CGD patients by allowing the use of haploidentical donor grafts without serious concerns of severe treatment-related toxicity.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s12185-015-1799-8DOI Listing

Publication Analysis

Top Keywords

model x-linked
8
chronic granulomatous
8
granulomatous disease
8
x-linked cgd
8
bone marrow
8
mixed chimerism
8
curative haploidentical
4
haploidentical bmt
4
bmt murine
4
murine model
4

Similar Publications

HP1 Promotes the Centromeric Localization of ATRX and Protects Cohesion by Interfering Wapl Activity in Mitosis.

Front Biosci (Landmark Ed)

January 2025

The Key Laboratory of Model Animals and Stem Cell Biology in Hunan Province, Hunan Normal University Health Science Center, 410013 Changsha, Hunan, China.

Background: α thalassemia/mental retardation syndrome X-linked (ATRX) serves as a part of the sucrose nonfermenting 2 (SNF2) chromatin-remodeling complex. In interphase, ATRX localizes to pericentromeric heterochromatin, contributing to DNA double-strand break repair, DNA replication, and telomere maintenance. During mitosis, most ATRX proteins are removed from chromosomal arms, leaving a pool near the centromere region in mammalian cells, which is critical for accurate chromosome congression and sister chromatid cohesion protection.

View Article and Find Full Text PDF

Mutations Causing X-Linked Recessive Oligodontia with Variable Expression.

Genes (Basel)

December 2024

Department of Pediatric Dentistry & DRI, School of Dentistry, Seoul National University, Seoul 03080, Republic of Korea.

Background/objectives: The ectodysplasin A () gene, a member of the tumor necrosis factor ligand superfamily, is involved in the early epithelial-mesenchymal interaction that regulates ectoderm-derived appendage formation. Numerous studies have shown that mutations in the gene can cause X-linked ectodermal dysplasia (ED) and non-syndromic oligodontia (NSO). Accordingly, this study aimed to identify the causative genetic mutations of the gene.

View Article and Find Full Text PDF

Background: X-linked hypophosphatemia (XLH) is a rare disorder characterized by elevated levels of fibroblast growth factor 23 (FGF-23), leading to hypophosphatemia and complications in diagnosis due to its clinical heterogeneity. Metabolomic analysis, which examines metabolites as the final products of cellular processes, is a powerful tool for identifying in vivo biochemical changes, serving as biomarkers of pathological abnormalities, and revealing previously uncharted metabolic pathways.

Methods: A multicenter cross-sectional case-control study of adult patients diagnosed with XLH was conducted.

View Article and Find Full Text PDF

Independent genetic strategies define the scope and limits of CDKL5 deficiency disorder reversal.

Cell Rep Med

January 2025

Department of Genetics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19102, USA; Department of Neuroscience, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19102, USA; The Epigenetics Institute, University of Pennsylvania, Philadelphia, PA 19102, USA. Electronic address:

Cyclin-dependent kinase-like 5 (CDKL5) deficiency disorder (CDD) is a neurodevelopmental syndrome caused by mutations in the X-linked CDKL5 gene. The early onset of CDD suggests that CDKL5 is essential during development, but post-developmental re-expression rescues multiple CDD-related phenotypes in hemizygous male mice. Since most patients are heterozygous females, studies in clinically relevant female models are essential.

View Article and Find Full Text PDF

One hundred thirty-four germ line PU.1 variants and the agammaglobulinemic patients carrying them.

Blood

January 2025

Division of Immunology and Allergy, Children's Hospital of Philadelphia; Department of Pediatrics, Perelman School of Medicine; Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States.

Leukopoiesis is lethally arrested in mice lacking the master transcriptional regulator PU.1. Depending on the animal model, subtotal PU.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!