The Cost of Legality: Navigating Labour Mobility and Exploitation in Malaysia

Through examining the experiences of Burmese migrant workers in Malaysia this paper analyses the complicated relationship between legal status and protection from violence and abuse. While legal status has often been promoted as a means to protect migrants, we suggest that legal status is actually pursued only at particular moments and on the basis of particular cost/benefit calculations made by migrants. Even as legal status offers some protection from state authorities, the linkage between legal status and employer sponsorship means that it also binds migrants to specific employers. Crucial to these calculations too is the cost of legal status for both migrants and employers, imbuing the relationship with financial risk on both sides and turning legal status into an expensive "commodity". Therefore, while migrant labour is often constructed as being "cheap", our study reveals that a key factor in the exploitation of migrants is that they are in fact so expensive to hire. Thus, as we argue here, it is important to look beyond a narrow focus on legal status and consider the basis on which such status is extended - especially as such status is increasingly predicated on a sponsoring employer and significant financial investments

CpG-induced tyrosine phosphorylation occurs via a TLR9-independent mechanism and is required for cytokine secretion

Toll-like receptors (TLRs) recognize molecular patterns preferentially expressed by pathogens. In endosomes, TLR9 is activated by unmethylated bacterial DNA, resulting in proinflammatory cytokine secretion via the adaptor protein MyD88. We demonstrate that CpG oligonucleotides activate a TLR9-independent pathway initiated by two Src family kinases, Hck and Lyn, which trigger a tyrosine phosphorylation–mediated signaling cascade. This cascade induces actin cytoskeleton reorganization, resulting in cell spreading, adhesion, and motility. CpG-induced actin polymerization originates at the plasma membrane, rather than in endosomes. Chloroquine, an inhibitor of CpG-triggered cytokine secretion, blocked TLR9/MyD88-dependent cytokine secretion as expected but failed to inhibit CpG-induced Src family kinase activation and its dependent cellular responses. Knock down of Src family kinase expression or the use of specific kinase inhibitors blocked MyD88-dependent signaling and cytokine secretion, providing evidence that tyrosine phosphorylation is both CpG induced and an upstream requirement for the engagement of TLR9. The Src family pathway intersects the TLR9–MyD88 pathway by promoting the tyrosine phosphorylation of TLR9 and the recruitment of Syk to this receptor