학술논문

Impaired chemotaxis and cell adhesion due to decrease in several cell-surface receptors in cathepsin E-deficient macrophages.
Document Type
Article
Source
Journal of Biochemistry. May2009, Vol. 145 Issue 5, p565-573. 9p. 7 Graphs.
Subject
*ASPARTIC proteinases
*IMMUNE system
*CELLS
*BACTERIAL diseases
*MACROPHAGES
*CHEMOTAXIS
*CELL adhesion
Language
ISSN
0021-924X
Abstract
Cathepsin E is an endo-lysosomal aspartic proteinase exclusively present in immune system cells. Previous studies have shown that cathepsin E-deficient (CatE–/–) mice display aberrant immune responses such as atopic dermatitis and higher susceptibility to bacterial infection. However, the mechanisms underlying abnormal immune responses induced by cathepsin E deficiency are still unclear. In this study, we found that the cell-surface levels of chemotactic receptors, including chemokine receptor (CCR)-2 and N-formyl peptide receptors (FPRs), were clearly diminished in CatE–/–macrophages compared with those in wild-type cells. Consistently, chemotaxis of CatE–/–macrophages to MCP-1 and N-formyl-methionyl-leucyl-phenylalanine was also decreased. Similar to the chemotactic receptors, the surface expressions of the adhesion receptors CD18 (integrin β2) and CD 29 (integrin β1) in CatE–/– macrophages were significantly decreased, thereby reducing cell attachment of CatE–/– macrophages. These results indicate that the defects in chemotaxis and cell adhesion are likely to be involved in the imperfect function of CatE–/–macrophages. [ABSTRACT FROM PUBLISHER]