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Transient Decrease of Circulating and Tissular Dendritic Cells in Patients With Mycobacterial Disease and With
Laura Dotta1, Donatella Vairo2, Mauro Giacomelli3
1Department of Pediatrics, A. Nocivelli Institute for Molecular Medicine, ASST Spedali Civili of Brescia, Brescia, Italy.
Frontiers in Immunology
|July 18, 2020
Summary
Autosomal dominant partial Interferon-γ receptor 1 (IFNγR1) deficiency can cause a temporary drop in dendritic cells (DCs) during mycobacterial infections. Monitoring DC counts may indicate treatment effectiveness in these patients.
Area of Science:
- Immunology
- Genetics
- Infectious Diseases
Background:
- Interferon-γ receptor 1 (IFNγR1) deficiency is a genetic cause of Mendelian Susceptibility to Mycobacterial Disease (MSMD).
- IFNγR1 signaling is vital for dendritic cell (DC) activation, maturation, and T cell priming against intracellular pathogens.
Observation:
- A patient with autosomal dominant (AD) partial IFNγR1 deficiency presented with disseminated Mycobacterium avium infection.
- Immunophenotyping revealed a significant reduction in circulating myeloid and plasmacytoid DCs during acute infection.
- Lymph node biopsy showed a profound depletion of tissue plasmacytoid DCs.
Findings:
- AD partial IFNγR1 deficiency is associated with transient decreases in both circulating and tissue DCs during active mycobacterial infection.
- DC counts normalized after successful antimicrobial therapy.
- Similar DC depletion was noted in another patient with AD partial IFNγR1 deficiency.
Implications:
- Monitoring dendritic cell counts may serve as a valuable indicator of treatment response in patients with AD partial IFNγR1 deficiency.
- This finding highlights the role of the IFNγR1 pathway in maintaining DC homeostasis during mycobacterial infections.
