嗜碱粒细胞组胺释放试验检测抗高亲和力IgE抗体及其受体

目的 探讨慢性荨麻疹的发生机制。方法 用嗜碱粒细胞组胺释放试验,检测慢性特发性荨麻疹患者的血清组胺释放活性。结果 32例中,有15例（46．9％）患者血清组胺释放活性增高,提示FcεR1抗IgE自身抗体的存在。结论 部分慢性荨麻疹的发生与自身免疫机制有关。     

Experimental study of serum substantia nigra neuron autoantibody and its effect in Parkinson disease patients

Parkinson disease(PD) is a neurodegenerativedisorder characterized by the loss of melanin-containing neurons in the substantia nigra parscompacta (SNpc ) and a reduction in striataldopamine.The cause of PD remains unknown,but itis related to genetic,environmentalfactors,etc.Someevidence[1] indicated that multiple mechanisms wereinvolved in the pathogenic procedure of PD,such asoxidative stress,susceptibility to neurotoxin,excitingamine acid toxicity,immune factorand apoptosis,etc.In immune …     

间接免疫荧光法及蛋白质印迹法对肺癌患者体内自身抗体的分析

目的：了解肺癌患者血清自身抗体阳性率、细胞内定位及荧光图形特点,探索自身抗体作为肿瘤樗物的可能性。方法：应用间接免疫荧光法（ｉｎｄｉｒｅｃｔ ｉｍｍｕｎｏｆｌｕｏｒｅｓｓｅｅｎｅｅ,ＩＩＦ）检测７７份肺癌以及１４０份不同年龄段正常人血清中自身抗体。提取人喉癌上皮细胞（Ｈｅｐ－２）蛋白抗原,采用蛋白质印迹法对８１份肺癌患者及５２份正常人血清进行分析。结果：肺癌组和对照组的自身抗体阳性率有显著差别,两     

Complexity of the immunoglobulin light chain V kappa 1 gene family in the New Zealand black mouse

The immunoglobulin light chain V kappa 1 gene family is polymorphic in murine inbred strains and this family has been subdivided into five sub-groups (V kappa 1A-E). The V kappa 1A sub-group contributes to approximately 2% of the total serum immunoglobulin light chains in several mouse strains. However, it has been reported that this sub-group is absent in New Zealand Black (NZB) mouse serum. Amino acid sequencing of myeloma proteins from this inbred mouse has shown that they belong to the V kappa 1B sub-group. We report here the structure of nine functional germline genes from NZB mice that have high homologies to the V kappa 1A, V kappa 1B, V kappa 1C, and V kappa 1D sub-groups. In addition, a novel germline gene representing the prototype of a new sub-group (designated V kappa 1F) has been identified. We have isolated different V kappa 1 germline genes from a single restriction fragment length polymorphism (RFLP) fragment, as well as identical V genes from two different RFLP migrating bands. Therefore, the complexity of the genes encoding the immunoglobulin variable region cannot be determined solely by RFLP analysis. Nucleotide sequence analysis of 16 V kappa 1 genes which code for NZB autoantibodies indicate that they belong to five different V kappa 1 sub-groups with five hybridomas (31%) expressing the V kappa 1A sub-group. Comparison of the sequences of V kappa 1 genes expressed in hybridomas with corresponding germline genes show no somatic mutations.     

GAD-Ab、ICA和IAA联合检测对成人隐匿性自身免疫性糖尿病的诊断价值（附138例分析）

目的 评价血清谷氨酸脱羧酶抗体(GAD—Ab)、胰岛细胞抗体(ICA)和胰岛素自身抗体(IAA)联合测定对成人隐匿性自身免疫性糖尿病(LADA)的诊断价值。方法 利用ELISA法测定138例临床诊断为2型糖尿病患者及46例健康者的血清GAD—Ab、ICA和IAA，并比较抗体阳性和阴性患者的临床特征。结果 临床诊断为2型糖尿病患者GAD-Ab和ICA的阳性率分别为20．3％和11．6％，与对照组比较差异有显著性(X^2=8．528，P=0．003；X^2=5．841，P=0．016)；IAA的阳性率8．0％。与对照组比较无显著性差异(X^2=1．902，P=0．168)。抗体阳性患者血清C肽水平较低。结论 胰岛自身抗体联合检测可提高LADA患者的检出率；LADA患者胰岛储备功能较差。     

Association of genetic polymorphisms and autoimmune Addison’s disease

Autoimmune Addison’s disease (AAD) is a complex genetic disease that results from the interaction of a predisposing genetic background with as yet unknown environmental factors. The disease is marked by the appearance of circulating autoantibodies against steroid 21-hydroxylase. Mutations of the autoimmune regulator gene are responsible for the so-called autoimmune polyendocrine syndrome type I (APS I), of which AAD is a major disease component. Among genetic factors for isolated AAD and APS II, a major role is played by HLA class II genes: HLA-DRB1^*0301-DQA1^*0501-DQB1^*0201 and DRB1^*04-DQA1^*0301-DQB1^*0302 are positively, and RB1^*0403 is negatively, associated with a genetic risk for AAD. The MHC class I chain-related gene A allele 5.1 is strongly and positively associated with AAD. Other gene polymorphisms contributing to genetic risk for AAD are MHC2TA, the gene coding for class II transactivator, the master regulator of class II expression, cytotoxic T lymphocyte antigen-4, PTPN22 and the vitamin D receptor.     

Fetal rejection: infertility and immunity

Defective reaction toward fetal alloantigens could result in both recurrent spontaneous abortions (RSAs) and recurrent early pregnancy failures (REPFs), the latter existing in couples with unexplained infertility and multiple failures of implantation after in vitro fertilization embryo transfer. Immunological mechanisms leading to RSA and REPF seem to be different, although both syndromes probably have a genetic background that has not been identified so far. Despite the fact that antiphospholipid syndrome is a well-established cause of repeated pregnancy loss, the role of different autoantibodies existing in RSA and REPF patients needs to be elucidated. Immunotherapy is believed to correct the detrimental immune reactions; however, its real effectiveness and safety for the treatment of distinct forms of pregnancy loss need to be reconsidered.     

Synergistic actions of pemphigus vulgaris IgG,Fas-ligand and tumor necrosis factor-α during induction of basal cell shrinkage and acantholysis

This study tested a recently proposed “Basal Cell Shrinkage” hypothesis of pemphigus acantholysis through a quantitative analysis of individual and cooperative effects of pemphigus vulgaris (PV) IgG, Fas-ligand (Fas-L) and tumor necrosis factor-α (TNFα) on keratinocyte (KC) volume (i.e. cell size) and adhesive properties. Exposure of KC monolayers and MatTek EpiDermFT? tissues cultures to the physiologic concentrations of Fas-L, TNFα or IgGs from two PV patients resulted in various degrees of reversible changes, which were not observed in control cultures either exposed to normal IgG or left intact. Within 12–24 h of exposure, basal cells in experimental cultures lost their ability to form stress fibers, retracted cytoplasmic aprons and formed keratin aggregates, indicating that their cytoskeleton collapsed. The cell volume decreased significantly (p < 0.05) as the polygonal cell shape changed to a round one. The shrunk cells detached from their neighbors and the substrate, resulting in a reciprocal increase of both the areas of acantholysis and the number of detached KCs, respectively. Since in the skin of PV patients, KCs are targeted by autoantibodies concomitantly with being exposed to autocrine and paracrine pro-apoptotic and pro-inflammatory cytokines, we combined PV IgG with Fas-L and/or TNFα in the cell culture experiments. This amplified several fold an ability of PV IgG to cause basal cell shrinkage and detachment. The obtained results demonstrated for the first time that PV IgG works together with Fas-L and TNFα to induce acantholysis via basal cell shrinkage, which provides a novel mechanism explaining successful treatment of PV patients with TNFα inhibitors.     

Innate immunity in self and infectious nonself recognition

Response to: Ameratunga R, Woon S-T, Gillis D et al. Challenges in diagnosis of CVID. Expert Rev. Clin. Immunol. 10(2), 000–000 (2014).