Anti-CD66b antibody [EPR7701]

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

CD66b also known as carcinoembryonic antigen-related cell adhesion molecule 8 (CEACAM8) is a glycoprotein with a molecular weight around 95 kDa. It is primarily expressed on the surface of granulocytes specifically on neutrophils—its expression on these cells makes it a useful marker in distinguishing stages of granulocyte maturation. The protein localizes to the cell membrane and serves as a cell adhesion molecule playing roles in intercellular interactions. Researchers often use CD66b-specific antibodies such as CD66b FITC for detecting and analyzing neutrophil populations commonly in flow cytometry applications.

Biological function summary

CD66b contributes to immune responses by facilitating leukocyte activation and migration during inflammation. It does not form part of a multi-protein complex but interacts with other cellular components. CD66b promotes neutrophil adhesion and transmigration to sites of infection or injury supporting their role in innate immunity. Additionally it participates in signaling pathways that influence cell survival proliferation and apoptosis in response to environmental cues.

Pathways

CD66b operates within neutrophil-related processes like the immune response and cell adhesion pathways. In the immune response pathway it collaborates with integrins to assist neutrophil extravasation through the endothelium. During inflammatory responses CD66b interaction with integrins and other adhesion molecules influences the intensity and duration of activity at inflammation sites. This interaction highlights its involvement with proteins such as ICAM-1 in mediating firm adhesion necessary for neutrophil migration.

Associated diseases and disorders

CD66b levels and activity correlate with conditions involving inflammation such as chronic obstructive pulmonary disease (COPD) and rheumatoid arthritis. During COPD the altered expression and regulation of CD66b contribute to neutrophil-driven inflammation exacerbating disease symptoms. Similarly rheumatoid arthritis involves inflammatory pathways where aberrant CD66b activity enhances synovial inflammation often linked with other inflammatory markers like TNF-alpha. Understanding CD66b's role in such diseases aids the development of therapeutic strategies targeting neutrophil-mediated pathology.