健康的細胞會表達出一種小RNA,，幫助它們回避來自免疫系統(tǒng)不必要的識別和進攻。在8月出版的《自然—免疫學》期刊上,，研究人員對這一機制進行了解釋,，并推測腫瘤可能也利用了同樣的機制來逃逸檢測。
在遇到病毒感染等壓力狀況時,，兩種蛋白質MICA和MICB會被免疫細胞上表達的受體NKG2D所識別,。對這些由壓力誘導的蛋白質的探測會觸發(fā)一種可去除壓力源的免疫反應。而病毒則會使用一種名為小RNA的短鏈RNA來抑制MICA和MICB的表達,，從而逃避相應的免疫反應,。
以色列希伯來大學Ofer Mandelboim和同事指出，類似于這種病毒,，健康的非壓力型人類細胞也能表達出抑制MICA和MICB表達的小RNA,，因此，健康細胞能逃避免疫系統(tǒng)的探測,。與健康組織相比,，人類的許多腫瘤組織也表達出過量的這類小RNA，從而讓它們逃過免疫系統(tǒng)的識別,，這就是問題的嚴重性所在,。 （生物谷Bioon.com）
生物谷推薦原始出處：
Nature Immunology，doi:10.1038/ni.1642,，Noam Stern-Ginossar,，Ofer Mandelboim
Human microRNAs regulate stress-induced immune responses mediated by the receptor NKG2D
Noam Stern-Ginossar1, Chamutal Gur1, Moshe Biton1, Elad Horwitz1, Moran Elboim1, Noa Stanietsky1, Michal Mandelboim2 & Ofer Mandelboim1
Abstract
MICA and MICB are stress-induced ligands recognized by the activating receptor NKG2D. A microRNA encoded by human cytomegalovirus downregulates MICB expression by targeting a specific site in the MICB 3' untranslated region. As this site is conserved among different MICB alleles and a similar site exists in the MICA 3' untranslated region, we speculated that these sites are targeted by cellular microRNAs. Here we identified microRNAs that bound to these MICA and MICB 3' untranslated region sequences and obtained data suggesting that these microRNAs maintain expression of MICA and MICB protein under a certain threshold and facilitate acute upregulation of MICA and MICB during cellular stress. These microRNAs were overexpressed in various tumors and we demonstrate here that they aided tumor avoidance of immune recognition.
1 Lautenberg Center for General and Tumor Immunology, The Hebrew University, The BioMedical Research Institute, Hadassah Medical School, Jerusalem 91120, Israel.
2 Clinical Virology Unit, Tel-Hashomer, Ramat Gan 52621, Israel.
