mProX™ Human CX3CR1 Stable Cell Line

Pokharel J, et al. "The cellular microenvironment regulates CX3CR1 expression on CD8(+) T cells and ." European journal of immunology, 2023.
The expression levels of the chemokine receptor CX3CR1 have been established as a precise marker for distinguishing different functional states of antigen-experienced T cells. However, the factors that affect CX3CR1 expression on T cells are not fully understood. Through their study, the authors demonstrate that in vitro priming of naive CD8(+) T cells is insufficient in inducing robust CX3CR1 expression, highlighting the limitations of this method in replicating in vivo T cell differentiation. Nonetheless, memory CD8(+) T cells generated in vivo were able to maintain CX3CR1 expression during culture. The authors then investigate the influence of various factors, such as TCR ligation, cell death, and CX3CL1 binding, on CX3CR1 expression. They find that TCR stimulation leads to the downregulation of CX3CR1, while exposure to factors released by necrotic cells, but not apoptotic cells, results in a selective disadvantage for CX3CR1(+) CD8(+) T cells. Finally, the authors demonstrate that exposure to CX3CL1 at physiological concentrations only minimally reduces CX3CR1 expression, thus allowing for accurate interpretation of T cell differentiation states marked by CX3CR1. These findings further reinforce the use of CX3CR1 surface levels as a reliable T cell differentiation marker and identify key factors that affect its expression and maintenance on CD8(+) T cells. Copyright protections apply to this article.
Pubmed: 37816219   DOI: 10.1002/eji.202350658

Mikosz A, et al. "Alpha-1 antitrypsin inhibits fractalkine-mediated monocyte-lung endothelial cell ." American journal of physiology. Lung cellular and molecular physiology, 2023.
Chronic obstructive pulmonary disease (COPD) is a condition characterized by persistent inflammation caused by damage to the lung's endothelial barrier and subsequent recruitment of white blood cells into the airspaces. One of the key mechanisms involved in controlling this recruitment is the interaction between the fractalkine ligand (CX3CL1) and its receptor (CX3CR1), which maintains a balance between endothelial and white blood cell interactions. Exposure to cigarette smoke and respiratory pathogens can increase the expression of enzymes that break down CX3CL1, but this process is inhibited by a protein called alpha-1 antitrypsin (AAT). However, the effect of AAT on this process during acute inflammation is not well understood. The aim of this study was to investigate the mechanism of CX3CL1 breakdown, its role in interactions between endothelial cells and white blood cells, and the impact of AAT on these interactions during acute inflammation. Experiments using mouse models and human cells showed that exposure to cigarette smoke and bacteria led to breakdown of CX3CL1 and increased recruitment of white blood cells. However, treatment with AAT was found to significantly reduce this recruitment. Furthermore, levels of broken-down CX3CL1 were found to be increased in individuals with COPD, and were associated with the level of emphysema in their lungs. These findings suggest that targeting CX3CL1 breakdown and augmenting AAT levels may be promising strategies for reducing excessive recruitment of white blood cells during both acute and chronic inflammatory conditions.
Pubmed: 37814796   DOI: 10.1152/ajplung.00023.2023