期刊
MUCOSAL IMMUNOLOGY
卷 1, 期 4, 页码 265-278出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2008.16
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资金
- Medical Research Council [P171/03/C1/048]
- National Institute of Health [NGA: 1 U01 AI070232-01]
- European Union [032296]
- MRC [G0400795] Funding Source: UKRI
- Medical Research Council [G0400795] Funding Source: researchfish
Inflammatory lung disease to innocuous antigens or infectious pathogens is a common occurrence and in some cases, life threatening. Often, the inflammatory infiltrate that accompanies these events contributes to pathology by deleterious effects on otherwise healthy tissue and by compromising lung function by consolidating (blocking) the airspaces. A fine balance, therefore, exists between a lung immune response and immune-mediated damage, and in some the threshold of ignorance may be set too low. In most cases, the contributing, potentially offending, cell population or immune pathway is known, as are factors that regulate them. Why then are targeted therapeutic strategies to manipulate them not more commonplace in clinical medicine? This review highlights immune homeostasis in the lung, how and why this is lost during acute lung infection, and strategies showing promise as future immune therapeutics.
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