瑞典研究人員日前發(fā)現(xiàn)了人體免疫系統(tǒng)的一種控制機(jī)制,，這一發(fā)現(xiàn)對治療多發(fā)性硬化癥、風(fēng)濕性關(guān)節(jié)炎及全身性紅斑狼瘡等免疫系統(tǒng)疾病有重要幫助,。
瑞典卡羅林斯卡醫(yī)學(xué)院3日在一份新聞公報中說，患有全身性紅斑狼瘡或其他免疫系統(tǒng)疾病的病人體內(nèi)缺少一種名為NKT的細(xì)胞,，他們的研究結(jié)果證明NKT細(xì)胞的減少是這些免疫系統(tǒng)疾病的主要致病原因,。
人體免疫系統(tǒng)中有一類特殊的細(xì)胞被稱為B細(xì)胞，當(dāng)人們患有免疫系統(tǒng)疾病時,，B細(xì)胞不但無法發(fā)揮作用,，反而會不斷分裂并傷害人體,。研究人員發(fā)現(xiàn),，NKT細(xì)胞直接控制著B細(xì)胞，指導(dǎo)它對人體組織產(chǎn)生影響,。當(dāng)人體內(nèi)缺少甚至沒有NKT細(xì)胞時,，B細(xì)胞會被錯誤地激活，傷害人體,。但當(dāng)NKT細(xì)胞廣泛存在時,，它能及時制止B細(xì)胞的錯誤“行為”，從而終止發(fā)病過程,。(生物谷Bioon.com)
生物谷推薦原文出處：
JEM doi: 10.1084/jem.20091314
Invariant NKT cells limit activation of autoreactive CD1d-positive B cells
Fredrik Wermeling1, Sara M. Lind1, Emilie Domange Jord?1, Susanna L. Cardell2, and Mikael C.I. Karlsson1
Faulty activation of autoreactive B cells is a hallmark of autoimmune diseases like systemic lupus erythematosus (SLE). An important feature restricting activation of autoreactive B cells is efficient removal of apoptotic material. Mounting evidence also connects a primary defect in invariant natural killer T (iNKT) cells to autoimmune disease development. However, exactly how this unconventional T cell subset is involved remains to be defined. Here, we identify a suppressive role for iNKT cells in a model where autoantibody production is triggered by an increased load of circulating apoptotic cells, resembling the situation in SLE patients. Absence or reduction of iNKT cells as well as absence of CD1d-expression on B cells, needed for direct iNKT–B cell interaction, leads to increased autoreactive B cell activation and symptoms of disease. The suppression mediated by the iNKT cells is observed before B cell entry into germinal centers and can be rescued by transferring iNKT cells to deficient mice. This links iNKT cells to handling of dying cells and identifies a novel peripheral tolerance checkpoint relevant for autoimmune disease. Thus, these observations connect two clinical observations in SLE patients previously considered to be unrelated and define a new target for immunotherapy.
