期刊
EXPERIMENTAL LUNG RESEARCH
卷 34, 期 7, 页码 391-407出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/01902140802221987
关键词
IP10; macrophage; MIG
资金
- NHLBI NIH HHS [R01-HL069442, R01 HL069422, F32 HL078110-01, F32-HL078110, F32 HL078110-02, R01 HL069442, R01 HL069422-04, T32-HL07287, F32 HL078110, T32 HL007287] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [T32HL007287, F32HL078110, R01HL069422, R01HL069442] Funding Source: NIH RePORTER
Th1 cells are implicated in numerous pulmonary inflammatory disorders, and adoptive transfer of alloreactive Th1 cells mediates lung injury and inflammation in mice. In response to Th1-mediated immune injury, CXCR3 ligands IP10 and MIG are markedly induced. Because Th1 cells express high levels of CXCR3, their recruitment and activity may be influenced by CXCR3 ligands. To examine the role of CXCR3 ligands, the authors inhibited CXCR3-ligand interaction by 2 approaches: (1) antibody ablation of CXCR3 ligands IP10 (CXCL10/interferon-gamma-inducible 10-kDa protein) and MIG (CXCL9/monokine-induced by interferon-gamma), and (2) use of cxcr3(-/-) mice. Antibody neutralization of IP10 and MIG reduced Th1-cell mediated lung inflammation but did not alter Th1-cell influx in the lung. In contrast, a lack of CXCR3 on host cells had no effect on Th1 cells influx or acute inflammation. In vitro, ablation of endogenous IP10 and MIG inhibited antigen-mediated Th1-cell proliferation. These results suggest that the influx of alloreactive Th1 cells into the lung does not require CXCR3 ligands, but that these chemokines do affect Th1-cell proliferation and activity within the affected tissue. Other CXCR3(+) leukocytes do not contribute to acute alloimmune injury.
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