Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ORGAN SPECIFICITY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources
PubMed1990

Vagal motor neurons innervating the stomach are site-specifically organized in the dorsal motor nucleus of the vagus nerve in rats.

The aim of the present study was to examine the neuroanatomical relationship between the brainstem and the stomach. For this purpose, by means of a horseradish peroxidase retrograde method, we identified the distribution of individual parasympathetic preganglionic neurons projecting to three specific gastric regions that have structural and functional differences in the rat stomach. Preganglionic neurons innervating the ventral forestomach were mainly distributed in the lateral part of the left dorsal motor nucleus of the vagus nerve, while those innervating both ventral corpus and antrum were chiefly located in the medial part of the left dorsal motor nucleus. On the other hand, preganglionic neurons projecting to the dorsal forestomach and the dorsal corpus and antrum were predominantly observed in the lateral and the medial part of the right dorsal motor nucleus, respectively. These results suggest that parasympathetic preganglionic neurons innervating the stomach are site-specifically organized in the dorsal motor nuclei.

Animals↗
PubMed1990

Immunogenetics of early-onset insulin-dependent diabetes mellitus among the Japanese: HLA, Gm, BF, GLO, and organ-specific autoantibodies--the J.D.S. study.

The Japan Diabetes Society (JDS) conducted a multicenter study on the immunogenetics of early-onset insulin-dependent diabetes mellitus (IDDM) of the Japanese. Human leukocyte antigen (HLA), properdin factor B (BF), immunoglobulin heavy-chain complex (Gm), and glyoxalase of erythrocytes (GLO) were typed, and organ-specific autoantibodies, including islet cell antibody (ICA), were assayed in 159 Japanese IDDM patients and their family members and in 258 healthy Japanese controls. The HLA-DRw9 phenotype and HLA-Bw61/DRw9 haplotype were significantly increased among the patients with autoantibodies other than ICA but with no autoimmune diseases (RR = 5.84, cP less than 0.001; and RR = 7.45, P less than 0.001), whereas the HLA-DR4 phenotype and HLA-Bw54/DR4 haplotype were significantly increased in those without either the autoantibodies or autoimmune diseases (RR = 2.64, cP less than 0.001; and RR = 4.55, P less than 0.001). The HLA-DR4 phenotype was significantly increased in the patients with autoimmune thyroid diseases (RR = 6.21, cP less than 0.05). In all groups of patients, the HLA-DR2 phenotype was significantly decreased, and the relative risk of the HLA-DRw9/DR4 genotype was highest among all HLA-DR genotypes. No significant association was found between HLA type and the duration or incidence of ICA. Gm types of g and gft were significantly increased in the patients with the autoantibodies (RR = 2.11, P less than 0.05; and RR = 34.11, P less than 0.05), whereas the BF-F phenotype was significantly decreased in the patients either with or without autoantibodies (RR = 0.43, P less than 0.05; and RR = 0.46, P less than 0.05). There was no association between IDDM and GLO type. These data indicate that immunogenetic bases underlying IDDM of the Japanese are heterogeneous, as are those in Caucasians.

Autoantibodies↗
PubMed2004

Prevalence of non-organ-specific autoantibodies in patients suffering from duodenal ulcer with and without Helicobacter pylori infection.

Autoimmunity, a feature of chronic infection by Helicobacter pylori, is first directed against gastric cells but is also associated with extragastric diseases. The aim of the present work was to look for the influence of the infection on induction of non-organ-specific autoantibodies (NOSAs). We compared 49 patients (28 males and 21 females; age range, 36-72 years; mean, 61 +/- 4.6 years) suffering from duodenal ulcer and H. pylori infection (Group A) to 38 subjects (20 male, 18 female; age range, 40-78 years; mean, 63 +/- 3.8 years) affected by duodenal ulcer related to the assumption of nonsteroidal antiinflammatory drugs (Group B). H. pylori infection was diagnosed by histology, 13C-urea breath test, and serum IgG antibodies. Autoimmunitary pattern was demonstrated by the presence of NOSAs in serum. Antinuclear (ANA), anti-smooth muscle (SMA), and anti-liver/kidney microsomal-1 (LKM-1) antibodies were present in 5 of 49 (10.2%), 2 of 49 (4%), and 0 Group A patients, respectively. In Group B, ANA was present in 3 of 38 (7.9%), SMA in 3 of 38 (7.9%), and anti-LKM-1 in 0 patients. The difference was not statistically significant. In this population, H. pylori infection is not associated with an increased prevalence of NOSAs.

Adult↗
PubMed2000

Role of genetic factors in organ-specific autoimmune diseases induced by manipulating the thymus or T cells, and not self-antigens.

There are accumulating demonstrations that manipulation of the T-cell immune system, such as elimination of a particular T-cell subpopulation from the periphery or removal of the thymus during a critical neonatal period, can elicit activation/expansion of pathogenic self-reactive T cells from the remaining T cells and produce a wide spectrum of organ-specific autoimmune diseases in otherwise normal mice or rats. The genetic makeup of the hosts appears to play a key role in determining which self-reactive T-cell clones are prone to be activated under such circumstances, since a comparable degree of the immunologic abnormality elicits autoimmune disease in different spectrums of organs, with different incidences and severities, depending on the mouse or rat strains used. These findings indicate that one aspect of natural immunologic self-tolerance is maintained by a T cell-mediated control of potentially pathogenic self-reactive T cells in the periphery, and that defective control, caused by environmental insults or genetic abnormalities, suffices to cause autoimmune disease; furthermore, in the presence of such a T-cell abnormality, host genetic factors including MHC and non-MHC genes may determine the specificity and intensity of the autoimmune responses, and consequently the phenotype of the autoimmune disease.

Animals↗
PubMed2005

CD4+CD25+ T cells prevent the development of organ-specific autoimmune disease by inhibiting the differentiation of autoreactive effector T cells.

Thymic-derived, naturally occurring, CD4+CD25+ regulatory T cells (nTreg) are potent suppressors of immune responses. A detailed understanding of which components of the development and activation of pathogenic effector T cells are inhibited by nTreg during the course of T cell-mediated, organ-specific autoimmunity is as yet unknown. We have analyzed the effects of polyclonal nTreg on the development of autoimmune gastritis. The nTreg inhibited the development of disease, but failed to inhibit the migration of effector cells into the gastric lymph node or stomach. Notably, nTreg did not inhibit the expansion of autoreactive T cells in the gastric lymph node. The primary effect of nTreg appeared to be inhibition of differentiation of autoantigen-specific T cells to Th1 effector cells, as reflected by a decrease in Ag-stimulated IFN-gamma production and a reduction in T-bet expression.

Adoptive Transfer↗
PubMed2000

[Organ-specific antibodies in children with idiopathic inflammatory bowel disease and their use in clinical practice].

BACKGROUND: Ethiopathogenesis of the idiopathic inflammatory bowel disease has not been yet fully explained. Several abnormalities of the humoral immunity supporting the concept of autoimmune character of the disease have been identified. The aim of our study was to characterise occurrence of the organ specific antibodies against the intestinal goblet cells and against acinar cells of the exocrine pancreatic tissue and to evaluate their significance for the diagnostics of the idiopathic inflammatory bowel disease. METHODS AND RESULTS: 69 children were included in the study. The group consisted of 20 patients with idiopathic proctocolitis (11 boys and 9 girls, 6 to 18 years old, average age 15.5) and 14 patients with Crohn's disease (9 boys and 5 girls, 5 to 18 years old, average age 14.7). Control group included 35 children (20 boys and 15 girls, average age 14.7). In patients of the idiopathic proctocolitis group, antibodies against the intestinal goblet cells were assayed by indirect immunofluorescence method in 55%. In patients with Crohn's disease, antibodies against acinar cells of the exocrine pancreatic tissue were found in 64.2%. Differences in manifestation of antibodies against acinar cells of the exocrine pancreatic tissue in Crohn's disease were statistically significant (p = 0.001). Statistically significant (p = 0.01) was also the difference of levels of antibodies against the intestinal goblet cells in patients with idiopathic proctocolitis when compared to patients with Crohn's disease. Statistically significant difference (p = 0.01) was found in levels of antibodies against acinar cells of the exocrine pancreatic tissue in Crohns disease and antibodies against the intestinal goblet cells in patients with idiopathic proctocolitis. CONCLUSION: Testing on presence of specific antibodies against acinar cells of the exocrine pancreatic tissue and against intestinal goblet cells is a valuable tool for the diagnostics of the idiopathic inflammatory bowel disease in childhood and adolescence.

Adolescent↗
PubMed2006

Organ specific autoantigens and the autoreactiveT cell repertoire: the case of myelin oligodendrocyte glycoprotein.

There is strong evidence that immunological self tolerance critically relies on the elimination of potentially autoaggressive T lymphocyte clones from the emerging immune repertoire during intrathymic T cell differentiation. These 'forbidden' T cells are deleted as a result of a confrontation with their specific self antigen as presented on medullary stroma cells. But this purging mechanism is remarkably leaky, allowing numerous autoreactive T cells to join the healthy immune repertoire. A paper in this issue of the European Journal of Immunology studies the effect of organ-specific autoantigen expression on the cognate T cell repertoire. Myelin oligodendrocyte glycoprotein (MOG), a putative autoantigen in human multiple sclerosis, is used as a model self antigen. T cell receptor profiles in wild-type mice were compared with those in MOG-knock-out mice. Surprisingly, significant differences were not found suggesting that, in this particular case, autoantigen expression does not affect the autoreactive T cell repertoire.

Animals↗
PubMed1987

Recognition of a purified Mr-40,000 organ-specific immunogen of human lung cancer by class II-restricted T-cells.

An Mr-40,000 polypeptide (p40) was purified from a lung cancer cell line on the basis of its antigenicity with leukocytes from lung cancer patients in an in vitro immunological assay of leukocyte adherence inhibition. Here, the cells and mechanism responsible for recognizing the purified p40 organ-specific cancer neoantigen (OSN) were studied. Buffy coat leukocytes from lung cancer patients showed a bell-shaped dose response with a peak response at 0.75 micrograms/assay. Mononuclear cells showed a similar response pattern, whereas pure T-cells were unreactive. Monoclonal antibodies (MAbs) to T-cell differentiation antigens T3 and T4 inhibited the response in a dose-dependent fashion, whereas anti-T8 had no effect, indicating T helper cells and their T3-antigen receptor complex recognized the antigen. MAbs to class II major histocompatibility complex (MHC) antigens also inhibited the response, whereas MAbs to class I MHC had no effect, indicating an important role for class II MHC antigens of monocytes. None of the MAbs inhibited the response to OSN on membrane fragments, which is mediated by antibody-dependent monocytes. Trypsin- or cyanogen bromide-cleaved p40 OSN triggered a response at the same concentrations as the intact molecule. The p40 OSN incubated with live leukocytes showed less than 30% proteolytic digestion. The results indicate that class II-restricted T-cells recognize, via their antigen-specific cell surface receptors, contiguous sequences within the immunogenic tumor molecule in the context of the molecule or peptides binding to class II transplantation antigens.

Antibodies, Monoclonal↗
PubMed2003

Substrate-dependent and organ-specific chloroplast protein import in planta.

The NADPH-dependent protochlorophyllide (Pchlide) oxidoreductase (POR) is unique because it is a photoenzyme that requires light for its catalytic activity and uses Pchlide itself as a photoreceptor. In Arabidopsis, there are three structurally related PORs, denoted PORA, PORB, and PORC. The import of one of them, PORA, into plastids of cotyledons is substrate dependent. This substrate dependence is demonstrated in intact seedlings of wild-type Arabidopsis and two mutants, xantha2, which is devoid of Pchlide, and flu, which upon redarkening rapidly accumulates Pchlide. In true leaves, PORA uptake does not require the presence of Pchlide. The organ specificity of the substrate-dependent import of PORA reveals a means of controlling plastid protein translocation that is closely associated with a key step in plant development, the light-dependent transformation of cotyledons from a storage organ to a photosynthetically active leaf.

Arabidopsis↗
PubMedDate not supplied

Genetics of allergic disease: evidence for organ-specific susceptibility genes.

BACKGROUND: While previous studies have probed the genetics of asthma and serum IgE levels, there have been no studies on the genetics of allergic conjunctivitis. This paper describes the initial phase of a genetic study of allergic conjunctivitis. METHODS: Approximately 117 families with probands with allergic conjunctivitis were recruited generating 245 affected sib pairs. Each family member completed a detailed questionnaire on atopic symptoms, and results from skin testing were obtained. Genomic DNA was extracted and genotyped using thirty-five polymorphic markers spanning human chromosomes 5, 6, 11, 12, 16 and 17. Heritability was assessed using the POINTER program, and nonparametric linkage analysis using the BETA program. RESULTS: Evidence for genetic linkage of allergic conjunctivitis was obtained for chromosomes 5, 16 and 17. Weak linkage was detected for chromosome 6 when studies were restricted to specific allergens. No evidence for linkage was detected for chromosomes 11 and 12. CONCLUSIONS: Consistent with heritability analysis discussed in this paper, genetic linkage for allergic conjunctivitis is shown to differ from that reported for atopic asthma. This indicates that there are likely to be organ-specific disease susceptibility genes, which together with general atopy genes target the allergic response to specific mucosal tissues.

Asthma↗
PubMed2004

Organ specificity, colonization and clearance dynamics in vivo following oral challenges with the murine pathogen Citrobacter rodentium.

Citrobacter rodentium belongs to a family of human and animal enteric pathogens that includes the clinically significant enterohaemorrhagic Escherichia coli (EHEC) and enteropathogenic E. coli (EPEC). These pathogens use attaching and effacing (A/E) lesions to colonize the host gastrointestinal tract. In this study we have used bioluminescence imaging (BLI) to investigate the organ specificity, dynamics of colonization and clearance of mice by C. rodentium in situ and in real time. The bioluminescent C. rodentium derivative, strain ICC180, expresses the luxCDABE operon from the entemopathogenic nematode symbiont Photorhabdus luminescens and light levels accurately reflect bacterial numbers both in vitro and in vivo. We have demonstrated that primary colonization of the mouse by C. rodentium takes place within the caecum, specifically within the specialized patch of lymphoid tissue known as the caecal patch. Following colonization of the caecum C. rodentium established a colonic infection. Clearance of C. rodentium ICC180 parallels the colonization dynamics, i.e. the caecum was first to be cleared followed by the colon. A bioluminescent eae (encoding the outer membrane adhesin intimin) C. rodentium mutant failed to establish long-term colonization, although low levels of bacteria could be recovered for up to 3 days post challenge from the caecum.

Adhesins, Bacterial↗
PubMed1975

Organ-specificity and diagnostic value of cell-mediated immunity against a liver-specific membrane protein: studies in hepatic and non-hepatic diseases.

In chronic active hepatitis (CAH, n=58) 70% of the HBsAg negative and 48% of the HBsAg positive cases showed a CMI against human liver specific proteins (HLPI). Using HBsAg as antigen only 12% of the HBsAg negative and 24% of the HBsAg positive cases gave a CMI response. On the basis of HBsAg and autoantibodies in the serum CAH patients could be divided into 4 subgroups. A close correlation between CMI against HLPI, sex, ANA and HL-A-8 could be detected. In a follow-up study of patients with acute virus B hepatitis (n=62) CMI against HBsAg was detected in 60% of the cases in the acute phase of the disease but in 15% only 3-6 months after the onset of the illness (n=40). In patients who developed a chronic HBsAg carrier status 3 of 5 cases remained persistently positive with HLPI as antigen in the migration inhibition test. - In non-hepatic diseases in which immunological abnormalities may be present (malignant diseases n=46, diabetes mellitus n=27, active tuberculosis, n=18 and untreated systemic lupus erythematodes, n=5) only 26% of patients with malignant diseases showed a migration inhibition with HLPI. - Using different antigens such as human liver specific proteins (HLP), rabbit liver specific proteins (RLP), brucella suis antigen and tuberculin it was possible to demonstrate the validity of the two-step migration inhibition test to detect CMI. The results with different antigens in hepatic and non-hepatic diseases demonstrated that cell-mediated immunity of HLPI is an organ specific immune reaction which is associated with acute and chronic active liver diseases as a time limited or long-lasting phenomenon. Positive reactions in some tumor patients suggest that different mechanisms may elicit an autoimmune reaction against liver antigens.

Antibodies↗
PubMed2007

Elevated serum BAFF levels in patients with localized scleroderma in contrast to other organ-specific autoimmune diseases.

Serum levels of B-cell activating factor belonging to the tumor necrosis factor family (BAFF), a potent B-cell survival factor, are elevated in patients with systemic autoimmune diseases, such as systemic lupus erythematosus (SLE), rheumatoid arthritis and systemic sclerosis (SSc). The objective of this study was to determine serum BAFF levels and relate the results to the clinical features in patients with organ-specific autoimmune diseases of the skin, such as localized scleroderma and autoimmune bullous diseases. Serum BAFF levels were examined by enzyme-linked immunosorbent assay in 44 patients with localized scleroderma, 20 with pemphigus vulgaris/pemphigus foliaceus, 20 with bullous pemphigoid and 30 healthy controls. Twenty patients with SSc and 20 with SLE were also examined as disease controls. Serum BAFF levels were elevated in localized scleroderma patients compared with healthy controls. Concerning localized scleroderma subgroups, patients with generalized morphea, the severest form of localized scleroderma, had higher serum BAFF levels than linear scleroderma or morphea patients. The BAFF levels of generalized morphea were comparable with those of SSc or SLE. Furthermore, serum BAFF levels correlated positively with antihistone antibody levels and the severity of skin lesion as well as the number of skin lesions. By contrast, serum BAFF levels were not significantly elevated in patients with pemphigus or pemphigoid. These results suggest that BAFF may be contributing to autoimmunity and disease development in localized scleroderma.

Adolescent↗
PubMed2002

Two new loci, PLEIADE and HYADE, implicate organ-specific regulation of cytokinesis in Arabidopsis.

In screens for regulators of root morphogenesis in Arabidopsis we isolated six new recessive mutants with irregular cell expansion. Complementation analyses placed the mutations in two loci, PLEIADE (PLE) and HYADE (HYA). Phenotypic analyses revealed multinucleated cells, cell wall stubs, and synchronized cell divisions in incompletely separated cells that are all characteristics of defective cytokinesis. These defects were pronounced in roots and undetectable in aerial organs. In addition, fertility and germination were not affected by the mutations. Thus, the alleles that we have isolated of PLE and HYA suggest that the genes may encode organ-specific components needed primarily during root development. Analysis of microtubule arrays during cell cycle in ple and hya roots indicates that the presence of several synchronized nuclei influences the position of preprophase band, mitotic spindles, and phragmoplasts. The enhanced and synergistic phenotype of PLE/ple.hya/hya seedlings and double mutants point to a role of PLE and HYA in the same process. These mutants provide tools to elucidate the regulation of nuclear cytoskeletal interactions during cell division and cytokinesis.

Arabidopsis↗
PubMed2005

Preventing organ-specific chemotherapy toxicity.

Recent advances in treatment for pediatric cancers has increased overall survival rates. As more and more survive pediatric cancer, we continue to see the emergence of late effects of treatment within pediatric and the growing adult survivor population. The evaluation of late effects was initiated approximately two decades ago, and has become an extremely important facet of pediatric oncology. This review delves into several of the most serious organ-specific late effects of pediatric cancer treatment, outline what we know and what we do not currently understand about preventing or reducing them. Clinical and bench research are necessary to develop interventions that will avoid or mitigate late effects and improve the health of pediatric cancer survivors.

Antineoplastic Agents↗
PubMed2006

The use of genomewide ENU mutagenesis screens to unravel complex mammalian traits: identifying genes that regulate organ-specific and systemic autoimmunity.

T-cell development is perhaps one of the best understood processes of mammalian cell differentiation, as many of the genes and pathways have been identified. By contrast, relatively little is known about the genes and pathways involved in immunological tolerance to self-antigens. Here, we describe the challenges associated with a genomewide screen designed at identifying new immune regulatory genes that uses a model of organ-specific autoimmunity leading to type 1 diabetes. The successful propagation and identification of the new gene variants will shed light on the various developmental checkpoints in lymphocyte development that are crucial for establishing tolerance to self-antigens.

Animals↗
PubMed1991

Organ-Specific and Environmentally Regulated Expression of Two Abscisic Acid-Induced Genes of Tomato : Nucleotide Sequence and Analysis of the Corresponding cDNAs.

The cDNAs, pLE4 and pLE25, represent mRNAs that accumulate in response to water deficit and elevated levels of endogenous abscisic acid in detached leaves of drought-stressed tomato (Lycopersicon esculentum Mill., cv Ailsa Craig) (A Cohen, EA Bray [1990] Planta 182: 27-33). DNA sequence analysis of pLE4 and pLE25 showed that the deduced polypeptides were 13.9 and 9.3 kilodaltons, respectively. Each polypeptide was hydrophilic, cysteine- and tryptophan-free, and found to be similar to previously identified proteins that accumulate during the late stages of embryogenesis. pLE4 and pLE25 mRNA accumulated in a similar organ-specific pattern in response to specific abiotic stresses. Yet, expression patterns of the corresponding genes in response to developmental cues were not similar. pLE25 mRNA accumulated to much higher levels in developing seeds than in drought-stressed vegetative organs. pLE4 mRNA accumulated predominantly in drought-stressed leaves. The similarities and differences in the accumulation characteristics of these two mRNAs indicates that more than one mechanism exists for the regulation of their corresponding genes.

Journal Article↗