Programmed Death-1 Inhibition of Phosphatidylinositol 3-Kinase/AKT/Mechanistic Target of Rapamycin Signaling Impairs Sarcoidosis CD4 + T Cell Proliferation

• Published in: American journal of respiratory cell and molecular biology Vol. 56; no. 1; pp. 74 - 82
• Main Authors: Celada, Lindsay J., Rotsinger, Joseph E., Young, Anjuli, Shaginurova, Guzel, Shelton, Debresha, Hawkins, Charlene, Drake, Wonder P.
• Format: Journal Article
• Language: English
• Published: United States American Thoracic Society 01.01.2017
• Subjects: Adult; Aged; Case-Control Studies; CD4-Positive T-Lymphocytes - immunology; Cell Proliferation; Demography; Female; Gene Expression Regulation; Humans; Male; Middle Aged; Original Research; Phosphatidylinositol 3-Kinase - metabolism; Programmed Cell Death 1 Receptor - metabolism; Proto-Oncogene Proteins c-akt - metabolism; Sarcoidosis - immunology; Sarcoidosis - metabolism; Sarcoidosis - pathology; Signal Transduction; TOR Serine-Threonine Kinases - metabolism; Young Adult; lymphocyte cell-specific protein-tyrosine kinase; AKT; sarcoidosis; programmed death-1; proliferation; phosphatidylinositol 3-kinase

Patients with progressive sarcoidosis exhibit increased expression of programmed death-1 (PD-1) receptor on their CD4 T cells. Up-regulation of this marker of T cell exhaustion is associated with a reduction in the proliferative response to T cell receptor (TCR) stimulation, a defect that is reverse...