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FAM83H Regulates Postnatal T Cell Development Through Thymic Stroma Organization.

Betul Melike Ogan1,2, Veronika Forstlova3, Laura Jane Dowling3

  • 1Laboratory of Transgenic Models of Diseases, Institute of Molecular Genetics of the Czech Academy of Sciences, Vestec, Czech Republic.

European Journal of Immunology
|January 16, 2026
PubMed
Summary
This summary is machine-generated.

The FAM83H protein is crucial for epithelial cell function and immune system development. Its deficiency in mice impairs thymic epithelial cell maturation, leading to reduced T cell production and developmental defects.

Keywords:
CK1FAM83HWnt/β‐catenin signaling pathwayimmune dysregulationlymphocytesthymic epithelial cellsthymic stromathymocytes

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Area of Science:

  • Molecular and Cellular Biology
  • Immunology
  • Developmental Biology

Background:

  • Family of Sequence Similarity 83H (FAM83H) is an epithelial cell protein interacting with casein kinase 1 (CK1) and keratins.
  • FAM83H mutations cause amelogenesis imperfecta, indicating its importance in enamel formation.
  • FAM83H regulates cytoskeletal organization, cell proliferation, and vesicular trafficking.

Purpose of the Study:

  • To investigate the role of FAM83H in mouse development and immune cell generation.
  • To characterize Fam83h-deficient mice and their thymic phenotypes.
  • To explore the molecular mechanisms underlying FAM83H's function in thymic epithelial cells.

Main Methods:

  • Generation of Fam83h-deficient mice (Fam83h-/-) and mice with a deleted CK1-binding domain (Fam83h∆87/∆87).
  • Phenotypic analysis of generated mouse models, including viability, coat, skin, and activity.
  • Assessment of lymphoid cell development, particularly T cell development in the thymus.
  • Single-cell transcriptomic analysis of thymic epithelial cells (TECs).

Main Results:

  • Fam83h-deficient mice exhibit subviability, smaller size, scruffy coat, scaly skin, weakness, and hypoactivity.
  • Deficiency in Fam83h leads to impaired lymphoid cell development, specifically a block in T cell expansion at the double-negative stage 3 (DN3) in the thymus.
  • Fam83h is expressed in thymic epithelial cells (TECs), and its absence disrupts thymic architecture and reduces T cell output.
  • Single-cell transcriptomics revealed reduced expression of the master regulator Foxn1 and its targets in cortical TECs (cTECs) of Fam83h-/- mice.

Conclusions:

  • FAM83H is essential for normal development, immune cell production, and thymic epithelial cell maturation.
  • FAM83H, potentially in conjunction with CK1, plays a critical role in regulating TEC function and thymic architecture.
  • These findings highlight FAM83H as a key regulator of T cell development through its impact on TECs.