| First Author | Chen H | Year | 2003 |
| Journal | Immunity | Volume | 19 |
| Issue | 1 | Pages | 95-104 |
| PubMed ID | 12871642 | Mgi Jnum | J:161042 |
| Mgi Id | MGI:4457025 | Doi | 10.1016/s1074-7613(03)00172-9 |
| Citation | Chen H, et al. (2003) Role for plastin in host defense distinguishes integrin signaling from cell adhesion and spreading. Immunity 19(1):95-104 |
| abstractText | Integrin ligation activates both cell adhesion and signal transduction, in part through reorganization of the actin cytoskeleton. Plastins (also known as fimbrins) are actin-crosslinking proteins of the cortical cytoskeleton present in all cells and conserved from yeast to mammals. Here we show that plastin-deficient polymorphonuclear neutrophils (PMN) are deficient in killing the bacterial pathogen Staphylococcus aureus in vivo and in vitro, despite normal phagocytosis. Like integrin beta2-deficient PMN, plastin-deficient PMN cannot generate an adhesion-dependent respiratory burst, because of markedly diminished integrin-dependent syk activation. Unlike beta2(-/-) PMN, plastin-deficient PMN adhere and spread normally. Deficiency of plastin thus separates the classical integrin receptor functions of adhesion and spreading from intracellular signal transduction. |
