Immunodeficiency reviews最新文献_第5页

AIDS vaccines: concepts and first trials. 艾滋病疫苗:概念和首次试验。

Immunodeficiency reviews Pub Date : 1989-01-01

P Sonigo, L Montagnier, P Tiollais, M Girard

引用次数: 0

The use of HLA-non-identical T-cell-depleted marrow transplants for correction of severe combined immunodeficiency disease. 使用hla -不相同的t细胞枯竭骨髓移植矫正严重的联合免疫缺陷疾病。

Immunodeficiency reviews Pub Date : 1989-01-01

R J O'Reilly, C A Keever, T N Small, J Brochstein

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Hereditary and acquired deficiencies of C1 inhibitor. 遗传性和获得性C1抑制剂缺陷。

Immunodeficiency reviews Pub Date : 1989-01-01

A E Davis

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Cytotoxic T lymphocytes in HIV-induced disease: implications for therapy and vaccination. 细胞毒性T淋巴细胞在hiv诱导的疾病:治疗和疫苗接种的意义。

Immunodeficiency reviews Pub Date : 1989-01-01

F Plata, G Dadaglio, N Chenciner, A Hoffenbach, S Wain-Hobson, F Michel, P Langlade-Demoyen

引用次数: 0

Leukocyte adhesion deficiency: molecular basis and functional consequences. 白细胞粘附缺陷:分子基础和功能后果。

Immunodeficiency reviews Pub Date : 1988-01-01

A Fischer, B Lisowska-Grospierre, D C Anderson, T A Springer

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Human immunodeficiency virus type 1 (HIV-1) infection of the nervous system: a review. 人类免疫缺陷病毒1型(HIV-1)感染神经系统:综述。

Immunodeficiency reviews Pub Date : 1988-01-01

J Michaels, L R Sharer, L G Epstein

{"title":"Human immunodeficiency virus type 1 (HIV-1) infection of the nervous system: a review.","authors":"J Michaels, L R Sharer, L G Epstein","doi":"","DOIUrl":"","url":null,"abstract":"Human immunodeficiency virus type I (HIV-1) is associated with a spectrum of neurological disorders. At the time of primary HIV-1 infection, an acute aseptic meningitis or encephalitis indicates central nervous system invasion. Evidence of HIV-1 infection is found in the CSF of most asymptomatic seropositive individuals, suggesting viral persistence in the nervous system. After a long incubation period, viral activation is signaled by expression of HIV-1 antigen in the CSF, which correlates with a profound dementia in adults or with an analogous progressive encephalopathy in children. The neuropathological substrate of this dementing process consists of multinucleated giant cells and diffuse white matter pallor. Immunocytochemical and in situ hybridization studies demonstrate that antigen presenting cells, including blood derived macrophages and resident brain microglia, are directly infected by HIV-1, and participate in the formation of the syncytial giant cells. Astrocytes and endothelial cells may also be infected, but evidence for infection of oligodendroglia and neurons is lacking. Studies of lentiviral encephalitides in ungulates and non-human primates emphasize the importance of specific viral antigenic stimulation and the role of inflammatory cells as direct or indirect mediators of tissue damage. The disorders of the peripheral nervous system described in patients with HIV-1 infection have not been convincingly linked to direct viral infection. At least two of the neuromuscular complications, the inflammatory motor neuropathy and polymyositis are likely to have an autoimmune pathogenesis.","PeriodicalId":77170,"journal":{"name":"Immunodeficiency reviews","volume":"1 1","pages":"71-104"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14211588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular genetics of chronic granulomatous disease. 慢性肉芽肿病的分子遗传学。

Immunodeficiency reviews Pub Date : 1988-01-01

M C Dinauer, S H Orkin

{"title":"Molecular genetics of chronic granulomatous disease.","authors":"M C Dinauer, S H Orkin","doi":"","DOIUrl":"","url":null,"abstract":"Chronic granulomatous disease is an inherited disorder characterized by the failure of phagocytic cells to produce superoxide upon the ingestion of microorganisms due to a lesion in a membrane-associated NADPH-oxidase. The components of the oxidase have been incompletely characterized by standard biochemical approaches. A genetic strategy has recently led to the identification of the gene affected in the common X-linked form of CGD without reference to its protein product. The X-CGD gene, assigned to chromosome position Xp21.1, encodes a phagocyte-specific RNA transcript that is mutated in patients with X-CGD. Antisera directed toward the predicted protein product of the X-CGD gene recognize a 90 kD membrane glycoprotein, which corresponds to the larger subunit of the phagocyte b-cytochrome heterodimer. The recent genetic and biochemical findings provide an explanation for the consistent absence of the b-cytochrome spectrum in X-CGD, and establish this cytochrome as an essential component of the phagocyte oxidase. The primary amino acid sequence of both the 90 kD b-cytochrome subunit and the 22 kD subunit (cloned as the cDNA using a specific antisera) have no significant similarity to other proteins, including previously studied cytochromes. As both subunits of the b-cytochrome heterodimer are absent in X-CGD, despite a genetic deficiency of only the larger polypeptide, a close interaction between the two subunits may be important for b-cytochrome stability and function. Expression of the b-cytochrome large subunit mRNA is increased by interferon-gamma, an important macrophage activator. Partial or complete restoration of oxidase activity in some X-CGD patients treated with interferon-gamma suggests new therapeutic approaches in the management of this disorder. Molecular reagents prepared from the cloned X-CGD cDNA or gene may prove to be clinically useful in prenatal diagnosis and may provide a basis for somatic gene therapy in future.","PeriodicalId":77170,"journal":{"name":"Immunodeficiency reviews","volume":"1 1","pages":"55-69"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14210747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

First description of an acquired immunodeficiency. 首次描述获得性免疫缺陷。

Immunodeficiency reviews Pub Date : 1988-01-01

F S Rosen, M Seligmann

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Inherited deficiency of the fourth component of human complement. 遗传性缺乏人体补体的第四部分。

Immunodeficiency reviews Pub Date : 1988-01-01

G Hauptmann, G Tappeiner, J A Schifferli

{"title":"Inherited deficiency of the fourth component of human complement.","authors":"G Hauptmann, G Tappeiner, J A Schifferli","doi":"","DOIUrl":"","url":null,"abstract":"The highly polymorphic fourth component of human complement (C4) is usually encoded by two genes, C4A and C4B, adjacent to the 21-hydroxylase (21-OH) genes, and is also remarkable by the high frequency of the null alleles, C4A*Q0 and C4B*Q0. Despite considerable structural homology, the gene products of the two loci differ in hemolytic activities, antigenic reactivities and covalent binding affinities to antigens and antibodies. Complete C4 deficiency is exceptional because this condition appears only in homozygotes for the very rare double-null haplotype C4AQ0,BQ0. In contrast, partial C4 deficiency is a common immune protein defect in all human populations as a consequence of the high frequency of the C4 half-null haplotypes. Complete C4 deficiency in most cases gives rise to SLE and an increased susceptibility to infections, and partial C4 deficiencies predispose to different auto-immune diseases related to extended HLA haplotypes bearing the C4 half-null haplotypes. Studies at the DNA level have shown that about half of the null alleles are due to deletions involving C4A and 21-OHA, C4B and 21-OHA or C4B and 21-OHB. Larger deletions including both C4A and C4B genes have never been observed. Partial C4 deficiency may be observed in combination with other complement deficiencies or immune defects, and allo- or auto-anti-C4 immunization is also a possible consequence of this genetic abnormality. Although the pathogenesis of the diseases related to complete and partial C4 deficiencies is not yet clearly understood, it is evident that C4 null alleles represent interesting markers and additive risk factors for autoimmune phenomena.","PeriodicalId":77170,"journal":{"name":"Immunodeficiency reviews","volume":"1 1","pages":"3-22"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14210745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Factors affecting the natural history of human immunodeficiency virus infection. 影响人类免疫缺陷病毒感染自然史的因素。

Immunodeficiency reviews Pub Date : 1988-01-01

A J Pinching

{"title":"Factors affecting the natural history of human immunodeficiency virus infection.","authors":"A J Pinching","doi":"","DOIUrl":"","url":null,"abstract":"Human immunodeficiency virus (HIV) establishes latent infection in CD4 lymphocytes and macrophages. It can destroy CD4 cells by direct virus cytotoxicity, indirectly through the host response against HIV-infected cells, or by both means. Cells of the macrophage lineage are generally not destroyed but can serve as a reservoir of virus. HIV also causes functional impairment in remaining infected and uninfected cells. After exposure to infection by sexual, blood or maternofetal contact, about half the contacts become infected with HIV. Factors influencing the inoculum derived from the infected person include type of contact, phase of infection and local factors enhancing HIV replication or excretion. In the exposed person, genetic factors and systemic or local events such as infection or inflammatory injury may influence relative susceptibility. After infection with HIV, a number of outcomes may be seen, including symptomless carriage, with or without lymphadenopathy, or symptomatic disease, including the AIDS-related complex, acquired immune deficiency syndrome and HIV encephalopathy. Infection, multiple pregnancy and infancy are associated with increased or more rapid progression to symptomatic disease; malnutrition and immunosuppressive drugs may exert a similar effect. Genetic factors appear to affect disease susceptibility. Mechanisms influencing progression can be divided into those affecting the rate of HIV replication, those that determine the host response to HIV, and those mediated by other immunosuppressive influences. The host's balance with HIV thus resembles that of a tightrope walker, any force tending to tip him towards a catastrophic and irretrievable decline.","PeriodicalId":77170,"journal":{"name":"Immunodeficiency reviews","volume":"1 1","pages":"23-38"},"PeriodicalIF":0.0,"publicationDate":"1988-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14045030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0