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ITGAL
ITGAL Full Name
Integrin, alpha L
ITGAL Introduction
ITGAL (Integrin alpha L), also known as CD11a, encodes a key adhesion molecule that forms the LFA-1 complex together with integrin beta 2. This receptor is predominantly expressed on leukocytes and plays a central role in immune cell adhesion, migration, and immunological synapse formation. Through binding to ICAM family members, ITGAL enables lymphocytes to firmly adhere to endothelial cells and antigen-presenting cells, a process that is essential for immune surveillance and effective immune responses. Because dysregulated immune cell trafficking and activation are hallmarks of many diseases, ITGAL has increasingly attracted attention as a biologically meaningful and clinically actionable target rather than a simple surface marker.

Functionally, ITGAL is deeply involved in shaping the tumor immune microenvironment. Multiple large-scale transcriptomic analyses have shown that ITGAL expression closely tracks with immune cell infiltration, particularly CD8⁺ T cells and NK cells, and with immune-related signaling pathways. In lung adenocarcinoma, higher ITGAL expression has been consistently associated with improved overall survival, progression-free survival, and disease-specific survival, suggesting that ITGAL reflects a more active anti-tumor immune contexture. Mechanistic studies further indicate that ITGAL can modulate cytokine expression in NK cells and influence immune checkpoint-related pathways, highlighting its potential relevance for predicting and enhancing responses to immunotherapy across different cancer types.
From a disease perspective, ITGAL displays context-dependent roles that are highly relevant for diagnosis and prognosis. In solid tumors such as colon adenocarcinoma, recent studies have demonstrated that ITGAL is significantly downregulated in tumor tissues compared with normal controls, and that lower expression correlates with higher metastatic risk and worse clinical outcomes, supporting its value as an early diagnostic and prognostic biomarker. Pan-cancer analyses reinforce this view, identifying ITGAL as a robust immunotherapy predictor across multiple malignancies. In contrast, in hematological cancers like acute myeloid leukemia, ITGAL is often overexpressed and associated with adverse prognosis, increased immunosuppressive cell infiltration, and enhanced leukemic cell survival, suggesting a tumor-promoting role in this setting. Together, these findings underscore ITGAL as a versatile immune-related target whose expression patterns can provide clinically meaningful insights into disease behavior, patient stratification, and therapeutic decision-making.
Alternate Names for ITGAL
ITGAL; integrin; alpha L (antigen CD11A (p180); lymphocyte function-associated antigen 1; alpha polypeptide); CD11A; LFA-1; LFA1A; integrin alpha-L; LFA-1A; LFA-1 alpha; integrin gene promoter; CD11 antigen-like family member A; lymphocyte function-associated antigen 1; leukocyte adhesion glycoprotein LFA-1 alpha chain; leukocyte function-associated molecule 1 alpha chain; antigen CD11A (p180); lymphocyte function-associated antigen 1; alpha polypeptide;
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