cAMP responsive element modulator α promotes effector T cells in systemic autoimmune diseases.
Emil CarlssonTaylor Cowell-McGloryChristian M HedrichPublished in: Immunology (2023)
T lymphocytes play a crucial role in adaptive immunity. Dysregulation of T cell-derived inflammatory cytokine expression and loss of self-tolerance promote inflammation and tissue damage in several autoimmune/inflammatory diseases, including systemic lupus erythematosus (SLE) and psoriasis. The transcription factor cAMP responsive element modulator α (CREMα) plays a key role in the regulation of T cell homeostasis. Increased expression of CREMα is a hallmark of the T cell-mediated inflammatory diseases SLE and psoriasis. Notably, CREMα regulates the expression of effector molecules through trans-regulation and/or the co-recruitment of epigenetic modifiers, including DNA methyltransferases (DNMT3a), histone-methyltransferases (G9a) and histone acetyltransferases (p300). Thus, CREMα may be used as a biomarker for disease activity and/or target for future targeted therapeutic interventions.
Keyphrases
- systemic lupus erythematosus
- disease activity
- oxidative stress
- poor prognosis
- dna methylation
- rheumatoid arthritis
- binding protein
- rheumatoid arthritis patients
- transcription factor
- ankylosing spondylitis
- cancer therapy
- juvenile idiopathic arthritis
- gene expression
- dendritic cells
- multiple sclerosis
- regulatory t cells
- drug delivery
- protein kinase
- immune response
- dna binding