Immune checkpoints play a critical role in maintaining the delicate balance of immune activation in order to prevent potential harm caused by excessive activation, autoimmunity, or tissue damage. B and T lymphocyte attenuator (BTLA) is one of crucial checkpoint, regulating stimulatory and inhibitory signals in immune responses. Its interaction with the herpes virus entry mediator (HVEM) plays an essential role in negatively regulating immune responses, thereby preserving immune homeostasis. In cancer, abnormal cells evade immune surveillance by exploiting checkpoints like BTLA. Upregulated BTLA expression is linked to impaired anti-tumor immunity and unfavorable disease outcomes. In preclinical studies, BTLA-targeted therapies have shown improved treatment outcomes and enhanced antitumor immunity. This review aims to provide an in-depth understanding of BTLA's biology, its role in various cancers, and its potential as a prognostic factor. Additionally, it explores the latest research on BTLA blockade in cancer immunotherapy, offering hope for more effective cancer treatments.
Keyphrases
- papillary thyroid
- immune response
- squamous cell
- poor prognosis
- oxidative stress
- public health
- dna damage
- induced apoptosis
- childhood cancer
- squamous cell carcinoma
- lymph node metastasis
- stem cells
- toll like receptor
- type diabetes
- adipose tissue
- cell cycle
- physical activity
- metabolic syndrome
- cell proliferation
- optical coherence tomography
- inflammatory response
- cell death
- endoplasmic reticulum stress
- cell cycle arrest
- long non coding rna
- climate change
- herpes simplex virus
- case control