bluuebunny/crossref_metadata_2025_split huggingface dataset:
Endoglin: a 180-kD endothelial cell and macrophage restricted differentiation molecule
Authors: O'CONNELL P J , McKENZIE A , FISICARO N , ROCKMAN S P , PEARSE M J , d'APICE A J F 
Published: July 2010

SUMMARYA MoAb RMAC8 was generated by immunizing Balb/c mice with cultured human umbilical vein endothelialcells (HUVE). The molecule recognized had a mol. wt of 180 kD non-reduced, 95 kD after reduction and 66 kD in its reduced and n-dcglycosylated form. Sequential immunoprecipilalion studies with the MoAb 44G4, which recognizes the o- and n-glycosylated homodimer endoglin, showed that both MoAbs recognize the same molecule on HUVE and phorbol myristate acetate (PMA)-stimulated U937 cells. The distribution of the RMAC8-recognized molecule was the same as that described for endoglin. i.e. arterial and venous endothelium, myelomonocytic and pre-B leukaemia cells and cell lines; however, unlike 44G4, RMAC8 also reacted weakly with monocytcs and strongly with in vitro differentiated macrophages as well as peritoneal and alveolar macrophages. This distribution of endoglin was confirmed by Northern blot analysis using a full length endoglin cDNA probe. These studies suggest that endoglin is a differentiation marker on macrophages.
A hereditary immunodeficiency characterized by CD8+ T lymphocyte deficiency and impaired lymphocyte activation
Authors: MONAFO W J , POLMAR S H , NEUDORF S , MATHER A , FILIPOVICH A H 
Published: July 2010

SUMMARY
An unusual form of severe combined immunodeficiency in children from two different families was associated with absence of CD8+ T lymphocytes and normal numbers of CD4+ T lymphocytes that did not respond to stimulation by non-specific mitogens, specific antibodies against the T cell receptor or specific antigens. The defect in the CD4+ cells was bypassed by activating agents which are independent of the T cell receptor. The combination of an activation defect and selective depletion of CD8+ T lymphocytes suggests that the defective pathway is important in the differentiation of immature thymocytes as well as the proliferation of mature lymphocytes.
Induction of adjuvant arthritis in mice
Authors: KNIGHT B , KATZ D R , ISENBERG D A , IBRAHIM M A , Le PAGE S , HUTCHINGS P , SCHWARTZ R S , COOKE A 
Published: July 2010

SUMMARYAdjuvant arthritis, induced by injections of Freund's complete adjuvant into the footpads of some rat strains, has been recognized as a useful animal model for many years. There has, however, been notable lack of success in reproducing this model in other species. We now describe the development of adjuvant arthritis in healthy strain mice approximately 2 months after injection of Freund's complete adjuvant. Although the clinical appearance of the mice and the joint histopathology closely resemble the adjuvant arthritis reported in the rat. we were unable to detect rheumatoid factor in sera from the affected animals. In parallel studies of T cell proliferation, affected animals responded to some mycobaclcrial antigens but not to the 65-kD heat shock protein of Mycobacterium tuberculosis, suggesting that some other epitope is important in the development of the disease.
Activated T-lymphocytes induce growth inhibition and prostaglandin E2 release from syngeneic glomerular mesangial cells
Authors: RADEKE H H , SCHWINZER B , RESCH K 
Published: July 2010

SUMMARYThe concept of an active role of T lymphocytes in the initiation and development of autoimmune glomerulonephritis has gradually evolved from recent investigations. In the present study we started in a murinc coculture system to directly examine cellular interactions of intrinsic glomerular mesangial cells (MC) and syngeneic T lymphocytes. Lymph node lymphocytes and. moreover, cloned T helper cells specifically affected syngeneic proliferating MC. causing growth inhibition and prostaglandin E2 (PGE2) release. The T cell specificity of mesangial cell responses was confirmed by demonstrating (i) that MC coculturcd with other cell types showed no reaction and (ii) that additional activation of T lymphocytes by IL-2 or concanavalin A significantly enhanced the MC responses. Subsequently, we confirmed the presence of T cell factors in the supernatants responsible for the observed effects: interferon-gamma (IFN-γ) and tumour necrosis factor (TNF). Experiments with combinations of recombinant mouse IFN-γ and human lymphotoxin or TNF-α showed that these lymphokines could substitute for the direct T lymphocyte effects causing a synergistic growth inhibition and PGE2 release from mouse MC. The observed lymphokine activities were not due to mesangiolysis as shown by neutral red uptake of MC. Pointing to the essential role of T helper cell-specific products, IFN-γ antibodies abolished both the IFN-γ and the combined IFN-γ/TNF-α effect. Thus, our investigations with syngeneic MC-lymphocyte cocultures demonstrated that cultured MC specifically responded to T lymphocytes and their products.
Antibodies to Mycobacterium paratuberculosis-specific protein antigens in Crohn's disease
Authors: ELSAGHIER A , PRANTERA C , MORENO C , IVANYI J 
Published: July 2010

SUMMARY
The possible role of infection with Mycobacterium paratuberculosis (MAP) for the etiopathogenesis of Crohn's disease (CD) has been a matter of long-term controversy. In addition to similarities with the pathology of ruminant paratuberculosis, DNA fingerprinting confirmed the organism isolated from gut tissue, but the specificity of the immune repertoire has not as yet been evaluated. We report here on a serological study of 29 patients with CD, 20 patients with ulcerative colitis and 18 healthy control subjects, using three antigens attributed with species-specificity and selective immunogenicity following MAP infection. Antibodies binding to the 38-kD band of MAP extract were demonstrable by the Western blot technique in 57% of CD patients. Antibody levels to the 24-kD (p24BCD) cathodic bands, determined by competition ELISA using a monospecific murine antiserum, and to the 18-kD protease-resistant purified bacterioferritin, delected by standard ELISA, were significantly elevated in 53% of CD patients. However, these three antibody specificities tested in individual CD patients did not show any correlation with each other. Thus, 18% of patients were positive for all three specificities, whilst 84% had antibodies to at least one of the specific antigens. Although the exact proportion of affected patients is yet to be defined, the serological results obtained support the view that MAP infection may play an ctiological role in Crohn's disease.
Expression and gene transcript of Fc receptors for IgG, HLA class II antigens and Langerhans cells in human cervico-vaginal epithelium
Authors: HUSSAIN L A , KELLY C G , FELLOWES R , HECHT E-M , WILSON J , CHAPMAN M , LEHNER T 
Published: July 2010

SUMMARYThe mechanism of transmission of HIV from the male to the female genital tract or in the reverse order is not clear. CD4 glycoprotein is the receptor for HIV and Langerhans cells and the related dendritic cells could play a role in the initial transmission of HIV. Fc receptors (FcR) for IgG might be involved in antibody-mediated binding of HIV. We carried out an immunohistological study of normal human cervical and vaginal epithelia for the presence of CD4 glycoprotein, Langerhans cells and FcR to IgG. CD4+ glycoprotein was not found in the vaginal or cervical epithelium, with the exception of a few endocervical epithelial cells. A small number of CD4+ mononuclear cells were found in the endocervical epithelium of a third of the specimens but a large number of CD4+ cells was found in the submucosa of most of the cervical and vaginal specimens. Langerhans cells expressing CD4, HLA class II, FcγR2 and FcγR3 were detected in most vaginal, ectocervical and transformation zone epithelia and in 9/14 endocervical tissues. FcγR3 was detected in about two-thirds of the columnar endocervical epithelium and the transformation zone. A smaller number of specimens expressed FcγR2 in these epithelia, but FcγRl was not detected. We then demonstrated mRNA for FcγR3 in the columnar endocervical epithelial cells and transformation zone by in situ hybridization, usinga CD16-RNA probe. FeγR3 and FcγR2 gene transcripts were also found in fetal cervical tissue by applying the polymerase chain reaction to amplify portions of the FcγR3 and FcγR2 coding sequences in cDNA prepared from fetal RNA. HLA-DR was found in the endocervical cells, transformation zone and in Langerhans cells of all specimens. The presence of Langerhans cells, Fcγ receptors and HLA class II antigen offers three potential mechanisms for cervico-vaginal HIV transmission: (i) direct HIV infection of Langerhans cells, (ii) binding of HIV antibody complexes to cervical epithelial Fcγ receptors and (iii) binding of HIV infected CD4+ cells to cervical HLA class II antigen which may infect these or the adjacent CD4+ cells.
HIV-induced deletion of antigen-specific T cell function is MHC restricted
Authors: MANCA F , NEWELL A , VALLE M , HABESHAW J , DALGLEISH A G 
Published: July 2010

SUMMARYWhen antigen-specific T cells are pulsed by antigen-presenting cells (APC) in the presence of HIV they are functionally deleted following subsequent exposure to syngeneic APC in the absence of HIV. Recombinant soluble HIV envelope (gp 120) is able to induce a similar effect which, unlike that induced by HIV, is reversible. Neither HIV nor gp120 affect the ability to respond to IL-2. Thus it is only antigen-specific responses involving the T cell receptor pathways and CD4/MHC class II interaction that appear to be inhibited by HIV-1 and gp120. Furthermore, the functional impairment caused by HIV-1 is specific to the T cells that respond to the antigen in co-culture with HIV, as there is no apparent effect on ‘bystander’-activated T cells specific for another antigen. Antigen-specific T cell lines may be deleted by A signalling mechanism which involves molecules other than gp120/CD4 but still requires MHC class II restriction.
Induction of intercellular adhesion molecule-1 (CD54) on human hepatoma cell line HepG2: influence of cytokines and hepatitis B virus-DNA transfection
Authors: VOLPES R , VAN DEN OORD J J , DESMET V J , YAP S-H 
Published: July 2010

SUMMARYHuman hepatocyte expression of intercellular adhesion molecule-1 (ICAM-1)(CD54) was studied in vitro by exposing the well differentiated human hepatoblastoma cell line HepG2 to various cytokines. In addition, hepatitis B virus (HBV)-DNA transfected HepG2 cells were also analysed. Expression of ICAM-1 on HepG2 cells was then revealed with an immunohistochemical procedure. Untreated HepG2 cells were unreactive, but showed strong cytoplasmic ICAM-1 immunoreactivity after treatment with interferon-gamma (IFN-γ). This induction was completely inhibited by addition of a neutralizing antibody directed to IFN-γ, IL-1, IL-6, tumour necrosis factor-α (TNF-α) and IFN-α used alone or in combination, did not induce ICAM-1 expression, neither did they inhibit the IFN-γ-induced expression of this adhesion molecule on HepG2 cells. Untreated hepatitis B virus-DNA transfected HepG2 cells expressed membranous ICAM-1. These results indicate that IFN-γ is the main cytokine trigger for ICAM-1 expression on HepG2 cells, suggesting that in areas of liver inflammation this adhesion molecule is up-regulated on hepatocytes by locally released IFN-γ. In addition, expression of ICAM-1 by hepatitis B virus-DNA transfected HepG2 cells suggests other, still unknown, triggering mechanisms in the induction of such adhesion molecules, for instance gene activation by viral genome, or autocrine virus-induced hepatocellular cytokine production.
Regulation of IL-2β receptor expression and β-chain mRNA by human thymocytes
Authors: REEM G H , HAN X , MARCELLI A 
Published: July 2010

SUMMARYThe high affinity form of the human IL-2 receptor (IL-2R) has two known components, the IL-2Rα (p55) and the IL-2Rβ chain (p75). We have previously shown that recombinant IL-2 (rIL-2) could induce the expression of the α-chain (p55) on T cells and thymocytes, and increase this expression following suboptimal activation with concanavalin A (Con A) in combination with IL-2. An increase in the accumulation of IL-2Rα-specific mRNA induced by rIL-2 in T cells and thymocytes had also been documented. We report here that the expression of IL-2Rβ on the cell surface can be demonstrated on human thymocytes by the binding of Mik β1, a MoAb directed against an epitope of the β-chain. The IL-2Rβ chain is constitutively expressed on freshly isolated thymocytes; this expression can be increased in thymocytes activated with Con A in combination with IL-2 or tetradecanoylphorbol 13-acetaie (TPA). Blocking the formation of high affinity receptors with a MoAb directed against the α-chain of the receptor results in an increase in the display of IL-2Rβ as evidenced by binding of MoAb Mik β1. The accumulation of IL-2Rβ specific mRNA is observed in freshly isolated thymocytes and it is increased in thymocytes cultured with rIL-2 alone, with Con A. and further enhanced by the addition of rIL-2 in combination with Con A or with TPA. Cyclosporine (CsA), which inhibits the accumulation of lymphokine-specific mRNA of thymocytes, does not inhibit the induction of the accumulation orIL-2Rβ-specific mRNA. This is analogous to its effect on the expression of the α-chain (p55), and the accumulation of α-chain-specific mRNA.
The expression of HLA-DR by monocytes from black and from white donors: different requirements for protein synthesis
Authors: MCPEEK M , SALKOWTTZ J , LAUFMAN H , PEARL D , ZWILLING B S 
Published: July 2010

SUMMARYEpidemiologic data indicates that blacks may be more susceptible than whites to infection by Mycobacterium tuberculosis. Resistance to the in vivo to growth of Mycobacteria in mice correlates with the persistence of MHC class II expression by peritoneal macrophages. The expression of HLA-DR by human monocytes from different groups of individuals also differs. The increase in the expression of HLA-DR by monocytes that occurs upon in vitro culture was prevented by the protein synthesis inhibitor cycloheximide (CHX) in a majority of black donors. In contrast, the increase in HLA-DR expression by monocytes from the majority of white donors was unaffected.
MHC restriction of synovial fluid lymphocyte responses to the triggering organism in reactive arthritis. Absence of a class I-restricted response
Authors: HASSELL A B , PILLING D , REYNOLDS D , LIFE P F , BACON P A , GASTON J S H 
Published: July 2010

SUMMARYSynovial fluid mononuclear cells (SFMC) from patients with reactive arthritis (ReA) show marked proliferative responses to preparations of the organism triggering the arthritis. Initial studies with MHC-specific MoAbs have indicated that a significant element of these proliferative responses is mediated by class II MHC-restricted CD4+ T cells. It is imperative to establish the presence or absence of a class I-restricted response, for two reasons. Firstly, the association of ReA with the MHC class I molecule. HLA B27, raises the possibility of there being a B27-restricted response to the triggering organism. Secondly, a number of the organisms associated with ReA are intracellular pathogens, whose antigens might be expected to be presented by class I MHC molecules. In an effort to identify a class I MHC-restricted pathogen-specific response in the SFMC of ReA patients, we have assessed the proliferative responses of SFMC depleted of CD4+ T cells. Responses were grossly diminished by CD4+ T cell depletion. We also investigated Chlamydia-specific cytotoxicity in the SFMC of patients with sexually acquired ReA in a system using productive chlamydial infection to produce both targets and effectors. Significant antigen specific cytotoxicity was not seen. These experiments do not provide evidence to support the existence of pathogen-specific responses by CD8+, class 1-restricted synovial fluid T cells in ReA.
Expression of antigen reactive with a monoclonal antibody to HTLV-1 P19 in salivary glands in Sjögren's syndrome
Authors: SHATTLES W G , BROOKES S M , VENABLES P J W , CLARK D A , MAINI R N 
Published: July 2010

SUMMARY
To examine the possible involvement of retroviruses in Sjögren's syndrome (SS), labial salivary gland sections from 99 individuals were probed with three MoAbs to core (gag) proteins of human T cell leukaemia virus-1 (HTLV-1) and two MoAbs to HIV-1. Sections from 31% of 39 patients with primary SS (pSS) contained an epithelial cytoplasmic protein reactive with a MoAb(197) to the p19 group specific antigen (gag) of HTLV-1. The antigen was also detected in samples from 24% of 17 patients with rheumatoid arthritis (RA) and SS. 21% of 14 patients with sicca symptoms and 12.5% of 16 patients with other connective tissue diseases. It was not found in the salivary glands of 13 normal controls. A second MoAb to p19 gag, a MoAb to the p24 gag of HTLV-1 and MoAbs to HIV-1 p17and p24 gags gave negative reactions. Serum antibodies to HTLV-1 were negative, confirming that the antigen was not part of HTLV-1. The antigen showed properties consistent with an endogenous retrovirus in that it was absent in healthy tissues or resting cells but inducible by stimulation with phytohaemagglutinin (PHA) or interferon-gamma (IFN-γ) It appeared to be distinct from the endogenous retroviral sequence HRES-1. These data suggest the presence of an endogenous retrovirus in salivary gland epithelium which could contribute to the chronic inflammation of SS.
Circulating intercellular adhesion molecule-1 (ICAM-1) antigen in sera of patients with idiopathic pulmonary fibrosis
Authors: SHIJUBO N , IMAI K , AOKI S , HIRASAWA M , SUGAWARA H , KOBA H , TSUJISAKI M , SUGIYAMA T , HINODA Y , YACHI A , ASAKAWA M , SUZUKI A 
Published: July 2010

SUMMARYIntercellular adhesion molecule-1 (ICAM-1), a member of immunoglobulin supergene family with a five-domain structure, is known to play an important role in inflammatory diseases. An ELISA was developed using two MoAbs against human ICAM-1 in order to detect the soluble shedding ICAM-1 antigen in sera. We measured levels of circulating ICAM-1 antigen in sera of patients with idiopathic pulmonary fibrosis (IPF), pulmonary sarcoidosis, hypersensitive pneumonitis, bacterial and mycoplasmal pneumonia, and inflammatory diseases of other organs. The results clearly demonstrated that IPF had significantly high levels of circulating ICAM-1 in sera as compared with other disorders or normal controls. Moreover, immunohistochemical analysis with MoAb against human ICAM-1 disclosed that in IPF, the expression of ICAM-1 was intensively enhanced on alveolar epithelial cells. These results suggest that ICAM-1 may contribute to the pathogenesis of IPF.
Spontaneous development of pancreatitis in the MRL/Mp strain of mice in autoimmune mechanism
Authors: KANNO H , NOSE M , ITOH J , TANIGUCHI Y , KYOGOKU M 
Published: July 2010

SUMMARYMRL/Mp mice are known to have autoimmune disease-prone genetic background, which contributes to the development of a lethal autoimmune disease at an early age in association with the lymphoproliferative gene, Ipr. In this study, we found that MRL/Mp mice, not bearing Ipr (MRL/Mp-+/+), spontaneously developed pancreatitis at a late stage of life, which was histopathologically characterized by destruction of pancreatic acinar cells with mononuclear cell infiltration. In female 34–38-weeks-old mice the incidence of pancreatitis reached 74%, whereas the male mice developed the disease with a reduced incidence, at a later stage of life and with a reduced severity. Cell infiltrates in the affected lesions were composed predominantly of CD4+ cells and to lesser extent Mac-2+ macrophages. Adoptive transfer of the spleen cells obtained from pancreatitis-bearing female mice generated pancreatitis in female normal mice, but not in the male mice. Transfer of the serum of pancreatitis-bearing mice failed to induce any pancreatic lesions. These findings indicate that pancreatitis in MRL/Mp-+/+ mice may be mediated by cellular autoimmune mechanism. This may present a useful concept for analysis of the developmental mechanisms of human chronic pancreatitis in an aspect of autoimmunity.
Elevation of activated γδ T cell receptor bearing T lymphocytes in patients with autoimmune chronic liver disease
Authors: WEN L , PEAKMAN M , MIELI-VERGANI G , VERGANI D 
Published: July 2010

SUMMARYTo study the possible role of T cells bearing the γδ T cell receptor (TCR) heterodimer in the pathogenesis of autoimmune chronic active hepatitis (AI-CAH) and primary sclerosing cholangitis (PSC) in children, we measured levels of γδ+ T cells in the peripheral blood, assessed the proportion of cells bearing the disulphide-linked (BB3+) and non-disulphide-linked (A13+) subtypes of the receptor, and studied the co-expression of TCR-γδ and the activation markers HLA-DR and IL-2 receptor (IL-2R), and the memory cell marker CD45RO. Percentage levels and absolute numbers of γδ+ T cells were higher in both groups of patients than in controls (P &lt;0.01), mainly as a result of an increase in both percentage levels and absolute numbers of the A13+ subtype (P &lt;0.001). Coexpression of IL-2R and TCR-γδ was not found in controls but was present in some patients with AI-CAH (four out of 17) and PSC (six out of 12) at low levels (median 2.3%, range 1.7–5.0%). Expression of HLA-DR on γδ+ T cells was similar in both groups of patients and controls. The majority of γδ+ T cells in children with AI-CAH and PSC also expressed CD45RO (74.7 ± 18.4% and 79.8±24.3%, respectively) at levels significantly higher than in controls (53.3±17.2%, P &lt;0.01). These results suggest that autoimmune liver diseases in children are associated with an expansion and activation of γδ+ T cells in the peripheral blood, which may be important in the pathogenesis of these disorders.
IL-8 as a circulating cytokine: induction by recombinant tumour necrosis factor-alpha
Authors: SHERON N , WILLIAMS R 
Published: July 2010

SUMMARYTumour necrosis factor-alpha (TNF-α) is a pivotal cytokine at the centre of a cascade of cytokines and inflammatory mediators which modulate the host response to infection and trauma, and in particular the metabolic changes resulting in shock and subsequent multi-organ failure. The cytokine IL-8–predominantly an activator and chemotactic factor for circulating polymorphonuclear neutrophil leucocytes–is produced in response to TNF-αin vitro, and high circulating levels of IL-8 are found in septic primates. We have studied the release of IL-8 into the circulation of subjects with chronic hepatitis B undergoing a 10 week pilot trial of recombinant TNF-α (rTNF-α) therapy in doses of 15-100 μg/m2, A marked dose-dependent increase in plasma IL-8 levels was seen commencing at 30-60 min after the start of rTNF-α infusion and peaking between 2 and 3 h (mean peak level 4300 ng/l). The temporal pattern of IL-8 production exactly echoed that of IL-6, another component of the cytokine cascade, but peak plasma levels of IL-8 were up to 17 times higher than those of IL-6. This study confirms in vitro data suggesting that IL-8 is a component of the acute circulating cytokine cascade with a potential role in the modulation of the acute immune and metabolic response to infection and trauma.