| First Author | Zanin-Zhorov A | Year | 2007 |
| Journal | J Immunol | Volume | 179 |
| Issue | 1 | Pages | 41-4 |
| PubMed ID | 17579019 | Mgi Jnum | J:149426 |
| Mgi Id | MGI:3848437 | Doi | 10.4049/jimmunol.179.1.41 |
| Citation | Zanin-Zhorov A, et al. (2007) Cutting edge: T cells respond to lipopolysaccharide innately via TLR4 signaling. J Immunol 179(1):41-4 |
| abstractText | LPS, a molecule produced by Gram-negative bacteria, is known to activate both innate immune cells such as macrophages and adaptive immune B cells via TLR4 signaling. Although TLR4 is also expressed on T cells, LPS was observed not to affect T cell proliferation or cytokine secretion. We now report, however, that LPS can induce human T cells to adhere to fibronectin via TLR4 signaling. This response to LPS was confirmed in mouse T cells; functional TLR4 and MyD88 were required, but T cells from TLR2 knockout mice could respond to LPS. The human T cell response to LPS depended on protein kinase C signaling and involved the phosphorylation of the proline-rich tyrosine kinase (Pyk-2) and p38. LPS also up-regulated the T cell expression of suppressor of cytokine signaling 3, which led to inhibition of T cell chemotaxis toward the chemokine stromal cell-derived factor 1alpha (CXCL12). Thus, LPS, through TLR4 signaling, can affect T cell behavior in inflammation. |
