Journal
BLOOD
Volume 106, Issue 10, Pages 3432-3439Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2005-04-1393
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Funding
- Medical Research Council [G108/380] Funding Source: Medline
- NHLBI NIH HHS [HL36028, HL53993] Funding Source: Medline
- NIAID NIH HHS [AI48126] Funding Source: Medline
- MRC [G108/380] Funding Source: UKRI
- Medical Research Council [G108/380] Funding Source: researchfish
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Inflammatory responses are controlled by T helper 1 (Th1) lymphocytes. An important function of this polarity is the ability of T cells to traffick appropriately in vivo. This differential trafficking is dependent upon the binding of P-selectin glycoprotein ligand-1 to P- and E-selectin on inflamed endothelium as well as the expression of specific chemokine receptors. Here we show that in the absence of T-box expressed in T cells (T-bet), selective migration of T cells in vivo is completely abrogated and that T-bet regulates the binding of CD4(+) T cells to P-selectin. T-bet is also required for the expression of the chemokine receptor CXCR3. Thus, T-bet controls Th1-cell migration to inflammatory sites, which has fundamental consequences for the control of immunologic disease.
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