다중혈관 관상동맥 환자에서 y-문합을 이용하여 양쪽 내흉동맥만을 사용한 우회술의 조기 성적

抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

[신간의 별자리x] 우리/미술, 그리고 ‘슬픔의 박물관’

RNA interference (RNAi) is the process of sequence-specific, post-transcriptional gene silencing in animals and plants, initiated by double-stranded RNA (dsRNA) that is homologous in sequence to the silenced gene. The mediators of sequence-specific messenger RNA degradation are 21- and 22-nucleotide small interfering RNAs (siRNAs) generated by ribonuclease III cleavage from longer dsRNAs. Here we show that 21-nucleotide siRNA duplexes specifically suppress expression of endogenous and heterologous genes in different mammalian cell lines, including human embryonic kidney (293) and HeLa cells. Therefore, 21-nucleotide siRNA duplexes provide a new tool for studying gene function in mammalian cells and may eventually be used as gene-specific therapeutics.

Duplexes of 21-nucleotide RNAs mediate RNA interference in cultured mammalian cells

Probability Distributions.- Linear Models for Regression.- Linear Models for Classification.- Neural Networks.- Kernel Methods.- Sparse Kernel Machines.- Graphical Models.- Mixture Models and EM.- Approximate Inference.- Sampling Methods.- Continuous Latent Variables.- Sequential Data.- Combining Models.

Pattern Recognition and Machine Learning

Much has been accomplished in identifying the molecules and genes responsible for T-cell recognition. We are now familiar with two distinct heterodimers, αβ and γδ, and we know that the former (at least) confers on a T cell the ability to recognize antigens complexed with specific molecules of the major histocompatibility complex (MHC) (Dembic et al. 1986; Saito and Germain 1987). Because of the recent solution of an MHC class I structure (Bjorkman et al. 1987a,b), its apparent generalization to class II molecules (Brown et al. 1988), as well as the similarity of T-cell receptor (TCR) primary sequences to immunoglobulins (Igs), we can guess a great deal about how they might interact (Chothia et al. 1988, Claverie et al. 1989; Davis and Bjorkman 1988; see also Bjorkman and Davis, this volume).

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TCR recognition and selection in vivo.

Systems immunology.

Four common sites of chromosome breakage have been observed in patients with ataxia-telangiectasia (AT): 7p14, 7q35, 14q11.2, and 14q32. These sites appear to coincide with the location of genes for the T-cell receptor subunits (alpha, beta, and gamma) and IGH. Each of these genes involves rearrangements of DNA for its expression, suggesting that an abnormal DNA processing enzyme or family of enzymes underlies this propensity for chromosomal breakage in AT patients. Such a defect could also explain the radiation hypersensitivity of AT fibroblasts. In view of these findings, it is perhaps surprising that AT patients do not manifest more severe immunological defects although they would explain the lack of uniformity of these defects from one patient to the next. Two other genes utilize DNA rearrangement, IGK (on chromosome 2p12) and IGL (on chromosome 22q11), and have not been noted previously to be involved in translocations in these patients. We report here a 2:14 translocation (p14:q32) in a phytohemagglutinin-stimulated lymphocyte from a patient with AT.

Neoplasia and chromosomal breakage in ataxia-telangiectasia: a 2:14 translocation.

Oligonucleotide sequences are provided coding for T-cell-specific antigen receptors or fragments thereof. The oligonucleotide sequences can be used as probes for detecting helper and cytotoxic T-cells, preparing and isolating DNA sequences encoding for the receptor polypeptide, and in constructions for expression of receptor polypeptides or fragments thereof. In addition, processing signals from the receptor subunits can be employed in conjunction with modified wild type oligonucleotide sequences or non-wild type oligonucleotide sequences.

T-cell receptor βsubunit polypeptides

Abstract The immune mechanisms that mediate synovitis and joint destruction in rheumatoid arthritis (RA) remain poorly defined. Although increased levels of CD8 + T cells have been described in RA, their function in pathogenesis remains unclear. Here we perform single cell transcriptome and T cell receptor (TCR) sequencing of CD8 + T cells derived from anti-citrullinated protein antibodies (ACPA)+ RA blood. We identify GZMB + CD8 + subpopulations containing large clonal lineage expansions that express cytotoxic and tissue homing transcriptional programs, while a GZMK + CD8 + memory subpopulation comprises smaller clonal expansions that express effector T cell transcriptional programs. We demonstrate RA citrullinated autoantigens presented by MHC class I activate RA blood-derived GZMB + CD8 + T cells to expand, express cytotoxic mediators, and mediate killing of target cells. We also demonstrate that these clonally expanded GZMB + CD8 + cells are present in RA synovium. These findings suggest that cytotoxic CD8 + T cells targeting citrullinated antigens contribute to synovitis and joint tissue destruction in ACPA+ RA. 

/pdf/cytotoxic-cd8-t-cells-target-citrullinated-antigens-in-2w695x3t.pdf

Mark M. Davis

Papers

TCR recognition and selection in vivo.

Systems immunology.

Neoplasia and chromosomal breakage in ataxia-telangiectasia: a 2:14 translocation.

T-cell receptor βsubunit polypeptides

Cytotoxic CD8+ T cells target citrullinated antigens in rheumatoid arthritis