Monocyte Surface-Bound IL-15 Can Function as an Activating Receptor and Participate in Reverse Signaling1
Monocyte Surface-Bound IL-15 Can Function as an Activating Receptor and Participate in Reverse Signaling1
复制标题
单核细胞表面结合的 IL-15 可充当激活受体并参与反向信号传导1
作者：
G. Neely;S. Epelman;L. Ma;P. Colarusso;C. Howlett;E. Amankwah;A. McIntyre;S. Robbins;C. Mody
IL-15是一种短链、四-α螺旋的细胞因子，与IL-2具有相同的生物学功能。IL-2和IL-15之间的一个显著差异是单核细胞在活化后在其细胞表面上表达IL-15的能力。在目前的研究中，我们研究了人单核细胞表面IL-15参与反向信号传导的能力。交联抗IL-15 Ab用作表面IL-15接合的替代配体。细胞表面表达的IL-15的连接诱导单核细胞粘附，这需要小分子量的活性。GTP酶。通过表面IL-15的反向信号激活了Rho-GT3 Rac 3。此外，发现细胞表面IL-15的参与激活了许多信号传导途径，包括细胞外信号调节激酶1/2和p38，并导致IL-8的分泌。IL-8的产生需要丝裂原活化蛋白激酶活性。因此，目前的研究已经确定，细胞表面IL-15不仅仅是一种配体;它可以作为受体发挥作用，并参与导致细胞粘附和产生炎性细胞因子的反向信号传导。
IL-15 is a short chain, four-α helix cytokine that shares some biological function with IL-2. One striking difference between IL-2 and IL-15 is the ability of monocytes to express IL-15 on their cell surface after activation. In the current study we have investigated the ability of human monocyte cell surface IL-15 to participate in reverse signaling. Cross-linking anti-IL-15 Abs were used as a surrogate ligand for surface IL-15 engagement. Ligation of cell surface-expressed IL-15 induced monocyte adhesion that required the activity of small m.w. GTPases. Reverse signals through surface IL-15 activated the Rho-GTPase Rac3. In addition, engagement of cell surface IL-15 was found to activate a number of signaling pathways, including both extracellular signal-regulated kinase 1/2 and p38, and resulted in the secretion of IL-8. IL-8 production required mitogen-activated protein kinase activity. Thus, the current study has established that cell surface IL-15 is more than just a ligand; it can function as a receptor and participate in reverse signaling that results in cellular adhesion and production of inflammatory cytokines.
蛋白激酶激活在 MHC II 类配体诱导 B 细胞粘附中的作用。
DOI：
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发表时间：
1992
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
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作者：
Fuleihan,R;Spertini,F;Geha,RS;Chatila,T
通讯作者：
Chatila,T
影响因子：
32.4
作者：
Lodolce, JP;Boone, DL;Ma, A
通讯作者：
Ma, A