梅尼埃病的相关免疫因素研究进展

梅尼埃病的病因至今仍未完全清楚，但近十几年，随着耳免疫学研究的进展和深入，大量实验研究和临床观察结果发现，在部分梅尼埃病患者的发病过程中，免疫学因素起着极其重要的作用，本文就国内外有关梅尼埃病的免疫学研究的新成就加以综述。     

甲状腺素对大鼠实验性自体免疫心肌炎的作用

实验选用清洁级F344/NSIc大鼠,腹腔内注射甲状腺素（10μg/100g体重）,观察甲状腺素对肌球蛋白诱导的实验性自体免疫心肌炎的作用,并用免疫荧光技术结合流式细胞仪分析甲状腺素对免疫反应的影响。结果显示,甲状腺素对肌球蛋白免疫所致的心肌坏死,炎性细胞浸润和纤维化没有明显的改善作用;甲状腺素可诱导外周血B淋巴细胞比例升高。但对辅助T细胞和抑制T细胞比例。辅助T细胞/抑制T细胞比率没有影响。     

性别与自身免疫性疾病

自身免疫性疾病在人群中感染率5-10%,具有明显的性别差异,女性患者显著高于男性,具体机制仍未研究清楚。研究发现,除了机体自身的遗传易感体质外,雌激素,微嵌合体和性染色体都与自身免疫性疾病发病有关。     

性别与自身免疫性疾病

自身免疫性疾病在人群中感染率5-10％,具有明显的性别差异,女性患者显著高于男性,具体机制仍未研究清楚。研究发现。除了机体自身的遗传易感体质外,雌激素,微嵌合体和性染色体都与自身免疫性疾病发病有关。     

检测抗核抗体谱对自身免疫性疾病的临床应用

目的:分析自身免疫性疾病患者抗核抗体谱检测结果,探讨抗核抗体谱检测在自身免疫性疾病诊断中的应用。方法:分别采用间接免疫荧光法和免疫印迹法检测130例自身免疫性疾病患者和20例健康人的ANA和抗核抗体谱。结果:ANA在各种自身免疫性疾病中均有一定的阳性检出率,ANA在SLE中的检出率最高,阳性率为89.6%,其次为ITP、MCTD和SS。抗核抗体谱中的各种自身抗体在不同的自身免疫性疾病中有不同的敏感性和特异性。结论:采用间接免疫荧光法对ANA的检测对自身免疫性疾病有重要的筛查意义,抗核抗体谱检测对自身免疫性疾病的诊断有重要意义。     

科学家发现自体免疫控制机制

美国和比利时科学家近日在小鼠免疫系统内发现了一个特殊的机制。关闭这一机制会导致自体免疫疾病产生。这一发现阐明了自体免疫性的产生过程，对于研究新的药物以加强对癌症、艾滋病等的免疫响应也有所启示。相关论文8月13日在线发表于《自然》杂志。     

PNAS：改造T细胞可抑制自体免疫疾病

研究发现,通过改造调节性T细胞,可以缓解自体免疫疾病。     

治疗自身免疫性疾病的抗细胞因子疫苗

抗细胞因子疫苗是针对疾病相关细胞因子而设计与构建的一类能激发体液免疫应答的主动免疫治疗性疫苗,是用于自身免疫性疾病的一种极具潜力的新型疗法。目前研究与开发的抗细胞因子疫苗主要有2 种类型,一种是通过偶联载体或直接修饰为细胞因子引入外源表位而构建的蛋白疫苗,另一种则是可表达细胞因子免疫原的核酸疫苗。这两类疫苗在临床前及临床研究中,对各种自身免疫性疾病均显现出治疗活性。简介各类抗细胞因子疫苗及其作用机制,综述用于治疗类风湿性关节炎、多发性硬化症、系统性红斑狼疮等各种自身免疫性疾病的抗细胞因子疫苗研究进展。     

自体免疫免疫细胞治疗技术之CIK细胞治疗癌症

近年来:自体免疫细胞治疗技术越来越广泛地被应用到临床治疗中。自体免疫细胞治疗技术是指从患者自身外周血等中分离单个核细胞,经过专项实验室进行细胞的活化与增殖后,回输入患者体内,直接杀伤肿瘤细胞或被病毒感染的细胞,同时起到调节和增强机体免疫功能的作用。随着自体免疫细胞治疗技术的发展,应用细胞因子诱导的杀伤细胞(cytokine induced killer cell,CIK细胞)进行恶性肿瘤治疗的临床试验也陆续开展。     

高盐摄取与自体免疫疾病有关

2个独立的研究小组得出了相同的令人吃惊的结论：盐浓度升高通过刺激产生白介素-17的辅助T（TH17）细胞从CD4＋T-细胞的生成来促进自体免疫疾病。Chuan Wu等人发现，盐浓度的增加在试管中和在活体叶1都会诱导小鼠T-细胞中“血清糖皮质激素激酶-1”（SGK1）和增强TH17分化。     

Early disease onset and increased risk of other autoimmune diseases in familial generalized vitiligo

Generalized vitiligo is an autoimmune disorder in which acquired white patches of skin and overlying hair result from autoimmune loss of melanocytes from involved areas. Although usually sporadic, family clustering of vitiligo may occur, in a non-Mendelian pattern typical of multifactorial, polygenic inheritance. Sporadic vitiligo is associated with autoimmune thyroid disease, pernicious anemia, Addison's disease, and lupus; these same disorders occur at increased frequency in patients' first-degree relatives. Here, we studied 133 'multiplex' generalized vitiligo families, with multiple affected family members. The age of onset of vitiligo is earlier in these 'multiplex' families than in patients with sporadic vitiligo. Affected members of the multiplex vitiligo families have elevated frequencies of autoimmune thyroid disease, rheumatoid arthritis, psoriasis, adult-onset insulin-dependent diabetes mellitus, pernicious anemia, and Addison's disease. Probands' unaffected siblings have elevated frequencies of most of these same autoimmune diseases, particularly if the proband had non-vitiligo autoimmune disease. Familial generalized vitiligo is thus characterized by earlier disease onset and a broader repertoire of associated autoimmune diseases than sporadic vitiligo. This mostly likely reflects a greater inherited genetic component of autoimmune susceptibility in these families. These findings have important implications for autoimmune disease surveillance in families in which multiple members are affected with vitiligo.     

Molecular basis of a selective C1s deficiency associated with early onset multiple autoimmune diseases

We have investigated the molecular basis of selective and complete C1s deficiency in 2-year-old girl with complex autoimmune diseases including lupus-like syndrome, Hashimoto's thyroiditis, and autoimmune hepatitis. This patient's complement profile was characterized by the absence of CH50 activity, C1 functional activity <10%, and undetectable levels of C1s Ag associated with normal levels of C1r and C1q Ags. Exon-specific amplification of genomic DNA by PCR followed by direct sequence analysis revealed a homozygous nonsense mutation in the C1s gene exon XII at codon 534, caused by a nucleotide substitution from C (CGA for arginine) to T (TGA for stop codon). Both parents were heterozygous for this mutation. We used the new restriction site for endonuclease Fok-1 created by the mutation to detect this mutation in the genomic DNA of seven healthy family members. Four additional heterozygotes for the mutation were identified in two generations. Our data characterize for the first time the genetic defect of a selective and complete C1s deficiency in a Caucasian patient.     

Autoimmune diseases and cardiovascular risk

There are more than 80 different autoimmune diseases which collectively affect 4–8% of the world’s population. In a recent study published in Lancet, Conrad et al. found that 19 autoimmune diseases are associated with a composite of cardiovascular disease (CVD). Inflammation promotes atherosclerotic CVD with psoriasis and rheumatoid arthritis recognized as CVD risk enhancers. New strategies are needed to identify and mitigate the impact of chronic inflammation on CVD-related morbidity and mortality.     

Fatal legionellosis in patients with malignant hematologic diseases

Pneumonia was present in 70/157 (44.6%) autopsied patients with malignant hematologic diseases. In 16/70 patients (22.9%), legionellae were found to be the causative agents by screening lung tissue specimens with the direct fluorescent antibody method. In 5/16 patients with Legionella pneumonia, in whom legionellosis had been suspected clinically, the diagnosis had already been established by serology, urinary Legionella antigen detection, and culture. These results provide evidence that legionellosis is an important pneumonia etiology in patients with malignant hematological diseases. Thus, Legionella diagnostics should be applied routinely, and antibiotics effective in the treatment of legionellosis should be added to the usual therapy in patients with etiologically unexplained pneumonias. In view of the common occurrence of relapses of Legionella pneumonia, antibiotic therapy should be continued for an extended period.     

Apoptosis and autoimmune diseases

Apoptosis is a process by which harmful or useless cells are eliminated. This process can be divided into two steps, death and engulfment. Molecules involved in apoptosis have been identified, and mouse lines deficient in these genes have been established. Among these deficiencies, those in the death receptor system or the engulfment of apoptotic cells cause systemic lupus erythematosus, whereas inefficient DNA degradation causes anemia by activating innate immunity, leading to death during embryogenesis. The apoptotic process and the diseases caused by defects in it are briefly reviewed.     

Use of antilymphocyte globulin in autoimmune nervous system diseases]

The pathogenetic bases for the indication of immunosuppression in multiple sclerosis are represented in a survey, rested upon experiences in the clinical compatability test of AHLG Dessau. The knowledge gained in animal experiments and epidemiology in recent years is considered and problems of membrane, slow-virus hypothesis, genetic problems and changes of immunoglobulins and lymphocytes are critically referred to.     

Diarrhea caused by Campylobacter in patients with hematologic diseases]

Diarrhoea caused by Campylobacter infection in two adult patients was observed: one with erythroleukemia, and another with non-Hodgkin lymphoma. An infection developed in both cases during the period of agranulocytosis and decreased specific immunologic response to cytostatics. In case of the second patient, it has also been due to the underlying disease. The course of the disease has been different in both patient. It was dramatic with high fever and multiple fetid stools in one patient, and mild, successfully treated within a few days, in the second.