Immune dysregulation syndrome with de novo CTLA4 germline mutation responsive to abatacept therapy.
Abatacept
CTLA4 germ line mutation
Primary immunodeficient disease
Rheumatoid arthritis
Journal
International journal of hematology
ISSN: 1865-3774
Titre abrégé: Int J Hematol
Pays: Japan
ID NLM: 9111627
Informations de publication
Date de publication:
Jun 2020
Jun 2020
Historique:
received:
25
11
2019
accepted:
21
01
2020
revised:
21
01
2020
pubmed:
30
1
2020
medline:
30
9
2020
entrez:
30
1
2020
Statut:
ppublish
Résumé
Regulatory T-cells (Tregs) are major mediators of mammalian self-tolerance via cytotoxic T-lymphocyte antigen 4 (CTLA4) signaling pathways. An immune dysregulation syndrome associated with heterozygous germline mutations in CTLA4 was recently reported. Clinical features include recurrent infections, systemic lymphadenopathy, various autoimmune conditions, hypogammaglobulinemia, and autosomal dominant inheritance, characteristic of primary immunodeficient disease (PID). PID symptoms are variable and few patients with sporadic de novo CTLA4 germline mutations have been described. Here, we report the case of a 26-year-old man with an immune dysregulation syndrome and a de novo CTLA4 germline mutation. The patient exhibited several clinical features associated with PID. Next-generation sequencing revealed a CTLA4 germline mutation, c.436G>A; p.G146R, in exon 2 of CTLA4. Sanger sequencing confirmed the patient was the only member of his family with this germline mutation. The patient was diagnosed with an immune dysregulation syndrome associated with de novo germline CTLA4 mutation, complicated by steroid-refractory rheumatoid arthritis. Treatment with abatacept, a CTLA4-immunoglobulin fusion molecule, was initiated, resulting in dramatic resolution of the patient's clinical symptoms. As PID with CTLA4 germline mutation is rare and patients may be under-diagnosed, physicians should be aware of the features of PID.
Identifiants
pubmed: 31993940
doi: 10.1007/s12185-020-02834-9
pii: 10.1007/s12185-020-02834-9
doi:
Substances chimiques
CTLA-4 Antigen
0
CTLA4 protein, human
0
Abatacept
7D0YB67S97
Types de publication
Case Reports
Journal Article
Langues
eng
Sous-ensembles de citation
IM