Shimizu Y, Ashman L K, Du Z, Schwartz L B
Department of Internal Medicine, Virginia Commonwealth University, Richmond 23298, USA.
J Immunol. 1996 May 1;156(9):3443-9.
Kit, the receptor for stem cell factor (SCF) and the product of the c-kit proto-oncogene, is expressed on fetal liver-derived mast cell progenitors when cultured with SCF. Decreased levels of Kit on the surface of human fetal liver-derived mast cells after exposure to recombinant human SCF were demonstrated by flow cytometry using the YB5.B8 mAb against Kit. Internalization of Kit along with SCF appears to be the principal means by which Kit is lost from the mast cell surface. Neither the beta 3-integrin CD51/CD61 (alpha v beta 3), nor the beta 1-integrins CD49d,e/CD29 (VLA-4 and -5) appeared to be internalized along with Kit-SCF complexes. Reappearance of Kit on day 28 fetal liver-derived mast cells is complete 3 days after exposure of the cells to SCF and is detectable by 2 days. Recovery requires new protein and new RNA synthesis, because Kit did not reappear if cycloheximide or actinomycin D was added to the cells. No substantial change in total Kit mRNA was detected during the resynthesis period, suggesting that post-transcriptional regulation of Kit production is involved. Internalization of Kit in mast cells exposed to soluble SCF may represent a negative regulatory mechanism for this receptor-ligand interaction and down-regulate mast cell properties such as degranulation to SCF.
干细胞因子（SCF）的受体Kit是c-kit原癌基因的产物，在与SCF一起培养时，在源自胎儿肝脏的肥大细胞祖细胞上表达。使用抗Kit的YB5.B8单克隆抗体，通过流式细胞术证实，暴露于重组人SCF后，人胎儿肝脏来源的肥大细胞表面的Kit水平降低。Kit与SCF一起内化似乎是Kit从肥大细胞表面丢失的主要方式。β3整合素CD51/CD61（αvβ3）和β1整合素CD49d、e/CD29（VLA-4和-5）似乎都不会与Kit-SCF复合物一起内化。在将源自第28天胎儿肝脏的肥大细胞暴露于SCF后3天，Kit完全重新出现，并且在2天时可检测到。恢复需要新的蛋白质和新的RNA合成，因为如果向细胞中添加环己酰亚胺或放线菌素D，Kit不会重新出现。在重新合成期间未检测到总Kit mRNA有实质性变化，这表明Kit产生的转录后调节参与其中。暴露于可溶性SCF的肥大细胞中Kit的内化可能代表了这种受体-配体相互作用的负调节机制，并下调肥大细胞的特性，如对SCF的脱颗粒作用。
