MIF regulates innate immune responses through modulation of Toll-like receptor 4

By T. Roger, J. David, M. Glauser, Thierry Calandra. Nature, 2001

619 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Hypoxia is a potential risk factor for chronic inflammation and adiponectin reduction in adipose tissue of ob/ob and dietary obese mice. (2007, background): “Study of MIF knockout mice suggests that MIF is required for normal function of macrophage ( 43 ).”
CD44 is the signaling component of the macrophage migration inhibitory factor-CD74 receptor complex. (2006, background): “We also tested the potential effect of the Src kinase inhibitor PP2 (Salazar and Rozengurt, 1999).”
Cytokines in Sepsis: Potent Immunoregulators and Potential Therapeutic Targets—An Updated View (2013, background): “Once secreted, MIF increases macrophage antimicrobial responses by increasing macrophage survival [83], elevating TLR4 expression on macrophages [162] and promoting macrophage inflammatory recruitment [75].”
Novel strategies for the treatment of sepsis (2003, background): “A recent study suggested that MIF regulates Toll-like receptor-4 expression on macrophage”
Cytokine-mediated inflammation in acute lung injury. (2003, background): “MIF not only potentiates the effects of endotoxin and gram positive bacterial products[47,48], but it is an essential regulator of macrophage responses to endotoxin through its regulatory effect on Toll-like receptor-4 expression [49].”