Journal of inflammation最新文献_第10页

Molecular medicine: cytokines in health and disease. 分子医学:健康和疾病中的细胞因子。

Journal of inflammation Pub Date : 1995-01-01

G M Shearer

引用次数: 0

Generation of nitric oxide and clearance of interferon-gamma after BCG infection are impaired in mice that lack the interferon-gamma receptor. 缺乏干扰素-γ受体的小鼠在卡介苗感染后一氧化氮的生成和干扰素-γ的清除都会受到影响。

Journal of inflammation Pub Date : 1995-01-01

R Kamijo, J Gerecitano, D Shapiro, S J Green, M Aguet, J Le, J Vilcek

{"title":"Generation of nitric oxide and clearance of interferon-gamma after BCG infection are impaired in mice that lack the interferon-gamma receptor.","authors":"R Kamijo, J Gerecitano, D Shapiro, S J Green, M Aguet, J Le, J Vilcek","doi":"","DOIUrl":"","url":null,"abstract":"Mice with a targeted deletion of either the interferon (IFN)-gamma gene or the IFN-gamma receptor gene (IFN-gamma R(0/0) mice) fail to survive infection with the Bacillus Calmette-Guerin (BCG) strain of Mycobacterium bovis. Here we show that resident peritoneal macrophages isolated 2 weeks after BCG infection from IFN-gamma R(0/0) mice produced significantly less nitric oxide (NO) than wild-type macrophages. However, the response to lipopolysaccharide (LPS) was not completely abrogated in the IFN-gamma R(0/0) macrophages. BCG infection of wild-type mice led to a marked increase in their urinary nitrite/nitrate levels, as previously described. This increase in urinary nitrite/nitrate was not detected in BCG- infected IFN-gamma R(0/0) mice, indicating that no other cytokine can replace IFN-gamma as a mediator of increased NO synthesis after BCG infection in the intact organism. A comparison of circulating levels of IFN-gamma in BCG-infected animals revealed that sera from IFN-gamma R(0/0) mice contained up to 66-fold more IFN-gamma than sera from identically treated wild-type mice. To determine if the higher levels of circulating IFN-gamma were due to increased IFN-gamma synthesis, we compared the amounts of IFN-gamma mRNA present in the spleens of BCG-infected wild-type and IFN-gamma R(0/0) mice. No increase in IFN-gamma mRNA levels was detected in the spleens from IFN-gamma R(0/0) mice. Since the generation of IFN-gamma protein in cultured spleen cells was also not increased in IFN-gamma R(0/0) mice, we conclude that clearance of IFN-gamma from the circulation is impaired in IFN-gamma R(0/0) mice, thus revealing a heretofore unrecognized important role for the IFN-gamma receptor in the regulation of IFN-gamma levels in the intact organism.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"46 1","pages":"23-31"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19800433","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

Comparative expression of TNF-alpha alleles from normal and autoimmune-prone MHC haplotypes. 正常和自身免疫易感性MHC单倍型中tnf - α等位基因的比较表达。

Journal of inflammation Pub Date : 1995-01-01

F Bazzoni, B Beutler

{"title":"Comparative expression of TNF-alpha alleles from normal and autoimmune-prone MHC haplotypes.","authors":"F Bazzoni, B Beutler","doi":"","DOIUrl":"","url":null,"abstract":"The tumor necrosis factor-alpha (TNF-alpha, or TNF) genes of NOD mice and NZW mice are reportedly underexpressed relative to the TNF genes of control mice in lipopolysaccharide (LPS)-induced peritoneal macrophages. These findings, as well as the well-known major histocompatibility complex (MHC) linkage of the TNF genes, have prompted speculation that mutations affecting expression of the TNF-alpha loci might represent a primary cause of autoimmune diseases. Differences in expression of the TNF genes in different strains of mice might result either from effects of cis-acting mutations or from differences in the cellular environment that operate in trans. To discriminate between these possibilities, we directly examined the relative contribution made by each of two different TNF alleles (one associated with an autoimmune-prone haplotype and the other not) to the pool of TNF mRNA within the cells of F1 hybrid mice. Reverse transcription-polymerase chain reaction (RT-PCR) was used to amplify a polymorphic fragment derived from the total pool of TNF mRNA present in LPS-induced peritoneal macrophages of hybrid animals produced by crossing BALB/c to non-obese diabetic (NOD), and New Zealand black (NZB) to New Zealand white (NZW). In both types of F1 hybrid, the two alleles were represented in nearly equal quantities at the mRNA level. It may be inferred that at all pretranslational levels, the NZW and NOD TNF alleles are functionally equivalent to the control alleles that were examined. Interstrain differences in responsiveness to LPS are therefore responsible for interstrain differences in TNF gene expression.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"45 2","pages":"106-14"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18588862","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

Gaining insights into the ontogeny and activation of T cells through the use of gene-targeted mutant mice. 通过使用基因靶向突变小鼠，深入了解T细胞的个体发生和激活。

Journal of inflammation Pub Date : 1995-01-01

T W Mak

{"title":"Gaining insights into the ontogeny and activation of T cells through the use of gene-targeted mutant mice.","authors":"T W Mak","doi":"","DOIUrl":"","url":null,"abstract":"T lymphocytes recognize peptides bound to major histocompatibility complex products through the alpha- and beta-chains of their T-cell antigen receptors (TcR). The interaction between T cells and target cells or antigen-presenting cells is also assisted by a series of other accessory cell surface proteins. Probably most characterized of these accessory molecules are CD4 and CD8, which are differentially expressed on helper and cytotoxic T-cell lineages, respectively. Upon engagement of ligands by these cell surface proteins, a series of signals are transduced intracytoplasmically via associated protein kinases, such as the lymphocyte-specific tyrosine kinase lck. Another component important to signaling is the cell surface tyrosine phosphatase CD45, which through alternative splicing occurs in different isoforms on various hematopoietic and lymphopoietic cells. Despite the complexity of the TcR, signals generated via these receptors are thought to be insufficient to fully activate T lymphocytes. Many investigators believe that collateral (costimulatory) signaling of the CD28 molecule and the TcR facilitates complete activation of T lymphocytes. In addition, immune responses are regulated by a number of cytokines and soluble factors. Finally, at a very basic level, transcriptional factors, such as those involved in controlling interferon production, are important in T-cell development and immune responses. In an attempt to better understand the roles of these molecules in T lymphocyte function and ontogeny, we generated a series of mutant mice with disruptions in the genes coding for these molecules. The following discussion reports on some of the findings observed with these mutant animals.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"45 2","pages":"79-84"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18589353","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

Cellular and molecular mechanisms of TNF protection in septic peritonitis. TNF保护脓毒性腹膜炎的细胞和分子机制。

Journal of inflammation Pub Date : 1995-01-01

B Echtenacher, L Hültner, D N Männel

引用次数: 0