LFA-1是淋巴细胞相关抗原，在炎症中发挥重要作用，但对肿瘤的作用尚不明确。我们发现LFA-1基因缺失小鼠T细胞亚群失衡，CD3+ T细胞增多，CD8+ T细胞减少；利用蛋白芯片筛查明确LFA-1缺失小鼠血清和肺组织中IL-1β增高。建立尾静脉肺转移模型发现：肿瘤转移数量明显增多、体积增大；恶性程度增加；生存率下降；脾脏p-ERK1/2上调。上述结果提示：LFA-1缺失促进肿瘤转移的机制可能与淋巴细胞增殖分化相关。我们据此假设：LFA-1缺失通过影响T细胞亚群上调IL-1β从而促进肿瘤转移的发生。我们将利用LFA-1缺失小鼠研究LFA-1如何调控T细胞亚群，以及对IL-1β等炎症因子的影响；并且通过建立肺癌尾静脉转移模型及临床肺癌标本，探讨LFA-1在肿瘤转移中的作用，并明确其分子机制。本项目旨在明确LFA-1在肿瘤中对T细胞等免疫细胞的调控作用，为肿瘤免疫治疗呈现新视角和奠定理论基础。

Lymphocyte function-associated antigen 1, LFA-1, plays an important role in inflammation, but the effect of LFA-1 on cancer remains unclear.Our preliminary results showed that an imbalance ratio of T cell subsets contributes to increased CD3+T cells and decreased CD8+ T cells in LFA-1 deficient mice. Additionally, protein array screening displayed increased IL-1β level in serum and lung tissue, and up-regulated p-ERK1/2 in spleen in LFA-1 deficient mice. Furthermore, LFA-1 deficiency mice presented a significant increase in tumor numbers, tumor sizes, malignancy, and reduced survival rate using tail vein pulmonary metastasis model.These results suggested that the mechanism underlying LFA-1 deficiency in promoting tumor metastasis is possibly related to T lymphocyte proliferation and differentiation. We hypothesized that LFA-1 deficiency regulates the ratio of T cell subsets and substantially, induces more IL-1β secretion, leading to tumor metastasis. We are planning to use LFA-1 deficient mice to study how LFA-1 regulates T cell subsets, and its effects on IL-1β and other inflammatory cytokines.Tail vein metastasis mice model and analyzing clinical lung cancer samples will be applied to clarify its molecular mechanism. The aim of this study is to investigate the role of LFA-1 in the regulation of T cells in tumor development and this information will provide a new perspective as well as a molecular basis for tumor immunotherapy.