bluuebunny/crossref_metadata_2025_split huggingface dataset:
When the Light of the Home is Abroad: Unskilled Female Migration and the Filipino Family
Authors: Asis Maruja Milagros B. , Huang Shirlena , Yeoh Brenda S.A. 
Published: July 2004

AbstractThe migration of women engaged in transnational domestic work reveals how the uneven impacts of globalisation have intruded into the micro‐world of families and households. In this age of globalisation and migration, family membership has become multisited or transnational, with members dispersed in space. The migration of workers and the separation this entails has raised challenges to notions and ideals of “being family”. Unlike other workers on the move, the migration of domestic workers has some distinctive characteristics. It can be framed in terms of women moving between families and households; workers whose departure from their family of origin and insertion into their family of employment reconstitute the structure and content of family relationships in both material and imagined ways. Drawing on in‐depth interviews conducted in the Philippines and Singapore, we explore how migrant women and their family members define and negotiate family ideals, gender identities and family relationships, given the family's transnational configuration. Our findings provide some support to the notion that individual members in transnational families resort to “relativising” in fashioning responses to their situation.
Gender and Migration Policies in Southeast and East Asia: Legal Protection and Sociocultural Empowerment of Unskilled Migrant Women
Authors: Piper Nicola 
Published: July 2004

AbstractThis paper is concerned with how existing migration policies affect individual migrant women's choices, in particular, with the advancement, or consolidation, of a migrants' rights perspective. The focus is thereby on those migrants classified as unskilled, who constitute the largest and most vulnerable category among migrants. The analysis of migration policies has conventionally been approached from a state/government‐centred viewpoint that sees states as the key actors. This paper, however, emphasises a larger number of actors ‐ governmental and non‐governmental ‐ as well as the power relations among them to argue that protection through “legal regulation” in the absence of actual implementation is an incomplete solution to alleviate unfair labour conditions that migrants in general, and migrant women specifically, experience. Measures designed to “protect” migrants must be accompanied by measures that empower them, a role that has largely been taken on by existing migrant worker non‐governmental organisations (NGOs). Focussing on intra‐Asian migration flows in which Southeast Asia is the main labour sender and East Asia the receiver of Southeast Asian migrants, the paper explores the nexus between law and civic activism in the specific subject area of international labour migration and its gender implications.
Cytolytic Capabilities of Lamina Propria and Intraepithelial Lymphocytes in Normal and Chronically Inflamed Human Intestine
Authors: Melgar S. , Hammarström S. , Öberg Å. , Danielsson Å. , Hammarström M.‐L. 
Published: July 2004

AbstractCell‐mediated lymphocyte cytotoxicity in ileum and colon of patients with ulcerative colitis (UC), Crohn's disease (CD) and controls was investigated. Frequencies of cells expressing perforin and Fas‐ligand (FasL) were determined by immunomorphometry. mRNA expression of perforin, granzyme B and FasL in T cells and subsets was assayed by reverse transcriptase‐polymerase chain reaction. Cytotoxicity of intraepithelial and lamina propria lymphocytes was analysed without ex vivo activation in three functional assays: (1) anti‐CD3‐dependent T‐cell receptor (TCR)‐/CD3‐mediated redirected cytotoxicity, (2) Fas‐/FasL‐mediated TCR‐/CD3‐independent cytotoxicity and (3) natural killer (NK) cell cytotoxicity. Inflammation in ileum of CD patients caused increased frequency of perforin‐expressing cells and enhanced perforin‐dependent TCR‐/CD3‐mediated cytotoxicity. In contrast, lymphocytes in the inflamed colon of UC or Crohn's colitis patients did not display this cytotoxicity nor did lymphocytes of normal colon. Normal colon lymphocytes showed spontaneous Fas‐/FasL‐mediated cytotoxicity. This activity was retained but not enhanced in inflamed UC colon. In contrast, a significant increase of FasL‐expressing cells was seen in situ. Inflammation did not induce NK cell activity in colonic lymphocytes. Intestinal lymphocytes comprise effectors active in two different cytolytic processes. ‘Classical’ cytotoxic T lymphocytes in small intestine and lymphocytes executing TCR‐/CD3‐independent FasL‐/Fas‐mediated killing of unknown biological role present throughout the intestinal mucosa. Ongoing normal cytolytic processes seem to be enhanced by chronic inflammation.
Anti‐Class II Antibodies, but not Cytotoxic T‐Lymphocyte Antigen 4–Immunoglobulin Hybrid Molecules, Prevent Rejection of Major Histocompatibility Complex Class II‐Negative Myeloma in T‐Cell Receptor‐Transgenic Mice
Authors: Dembic Z. , Hofgaard P. O. , Omholt H. , Bogen B. 
Published: July 2004

AbstractWe have previously shown that tumour‐specific CD4+ T cells protect against subcutaneous injections of major histocompatibility complex (MHC) class II‐negative MOPC315 myeloma cells. Here, we have interfered with the immunologic events that lead to successful rejection of MOPC315 challenges in T‐cell receptor (TCR)‐transgenic mice. The CD4+ T cells have a transgene‐encoded TCR specific for a MOPC315 V‐region idiotypic (Id) peptide presented on the MHC class II molecule Ed. A side‐by‐side comparison indicated that DNA‐recombination‐deficient TCR‐transgenic mice were better protected against MOPC315 tumour development than recombination‐sufficient counterparts, suggesting that B cells or endogenous TCR chains might facilitate tumour progression in this model. Intraperitoneal injections of Ed‐specific antibodies over a period of initial 24 days, abrogated protection against tumours in both strains of mice. By contrast, injections of anticostimulatory molecules (cytotoxic T‐lymphocyte antigen 4–immunoglobulin hybrid molecules) had no effect. The findings demonstrate that tumour rejection depends on the presence of MHC class II molecules, despite the fact that MOPC315 tumour cells themselves do not express them. The results are consistent with the idea that secreted myeloma protein is processed and presented by class II+ antigen‐presenting cells to Id‐specific naïve CD4+ T cells that become activated and kill the myeloma cells by a bystander mechanism. While Id presentation on class II molecules is absolutely required for tumour rejection, costimulatory CD80/CD86 molecules might be dispensible in this process.
The Potential Role of Mannan‐Binding Lectin in the Clearance of Self‐Components Including Immune Complexes
Authors: Saevarsdottir S. , Vikingsdottir T. , Valdimarsson H. 
Published: July 2004

AbstractMannan‐binding lectin (MBL) is a pattern recognition receptor in the innate immune system. It recognizes certain sugar residues arranged in a pattern that enables MBL to bind with sufficient strength. Such sugar patterns are common on the surface of many microorganisms, and MBL has therefore been considered to be an agent that can discriminate between self and nonself. There is, however, increasing evidence supporting that MBL, like many membrane‐bound C‐type lectin‐like receptors, also helps to dispose of various outworn or abnormal body components. Most self‐components are protected with sialic acid or galactose that disrupt the pattern of the sugars that MBL can bind, but MBL may be significantly involved in the elimination of self‐components that have lost these protective terminal residues. The role of MBL in the clearance of invading pathogens has previously been thoroughly reviewed. Here, we review some findings that support the notion that MBL may contribute to noninflammatory removal of immune complexes and abnormal cells by the reticuloendothelial system. Defects in this clearance mechanism may cause an accumulation of potentially dangerous self‐components, thereby increasing the likelihood of chronic inflammation and autoimmunity.
Statin Drugs Do Not Affect Serum Complement Activation In Vitro
Authors: Lappegård K. T. , Hvassing T. , Mollnes T. E. 
Published: July 2004

AbstractStatin drugs prevent coronary heart disease through anti‐inflammatory mechanisms in addition to the well‐known reduction of low‐density lipoproteins. The complement system plays an essential role in the inflammatory response and has been postulated to be modified by statins. A direct role for statins in complement activation, however, has not been previously investigated. We therefore studied the effect of statins on in vitro complement activation. Pravastatin, atorvastatin and the active metabolite of the latter, ortho‐hydroxy atorvastatin, were added to normal human serum and incubated for 1 h in the absence or presence of aggregated immunoglobulin (classical pathway activation) or cobra venom factor (alternative pathway activation). The degree of complement activation, as detected by specific complement‐activation products for the classical pathway (C1rs‐C1‐inhibitor complexes), the combined classical and lectin pathway (C4bc), the alternative pathway (C3bBbP) and the final common pathway (C3bc and TCC), was not affected by pre‐incubation of the serum with any of the statins. Statins do not affect complement activation directly, but indirect effects in vivo may well be operative.
Apoptotic Effect of Rituximab on Peripheral Blood B Cells in Rheumatoid Arthritis
Authors: Szodoray P. , Alex P. , Dandapani V. , Nakken B. , Pesina J. , Kim X. , Wallis G. L. , Wilson P. C. , Jonsson R. , Centola M. 
Published: July 2004

AbstractRituximab (RTX) has proven efficacious in the treatment of rheumatoid arthritis (RA). Herein, we assessed the apoptosis‐inducing capability of RTX in vitro on RA peripheral blood B‐cell subsets and also compared the effects of RTX on B cells from rheumatoid factor‐positive (RF+) and RF– patients. The likely relevance of B cells in disease was assessed by measuring B‐cell‐modulating serum cytokines. Peripheral blood B cells were isolated and cultured with the presence or absence of RTX. The levels of apoptosis within the naïve, memory and IgD+CD27+ B‐cell subpopulations were determined by cytofluorometric analysis and caspase 3/7 assays. Levels of serum cytokines were measured with a multiplex cytokine array system. RTX induced significant apoptosis in all B‐cell subsets in both RA and controls. In naïve and memory B cells from RA patients, RTX induced significantly higher levels of apoptosis than in controls. RTX induced apoptosis of B cells in RF+ and RF– patients. Serum levels of interleukin‐1β (IL‐1β), IL‐4, IL‐10 and IL‐13 were profoundly increased in RF+ patients compared to RF− patients and controls. Although our cohort was small (10 RA patients), the data suggest that RTX induces apoptosis in all investigated subsets of B cells from RA patients. Interestingly, memory B cells from RA patients were more sensitive to RTX than memory cells from normal controls, suggesting that the delay in treatment response to RTX observed in clinical trials may be due in part to memory cell depletion. The apoptotic effects of RTX were similar in RF+ and RF– patients, but serum levels of B‐cell‐activating cytokine levels were only elevated in RF+ but not RF– patients. These data suggest that RTX is less effective in RF– RA because B cells play a less significant role in RA pathogenesis in RF– patients.
Interleukin‐2, But Not Interleukin‐15, is Required to Terminate Experimentally Induced Clonal T‐Cell Anergy
Authors: Bendiksen S. , Rekvig O. P. 
Published: July 2004

AbstractIt has been demonstrated that T cells stimulated with nucleosome–polyomavirus T‐antigen (self–nonself) complexes, but not nucleosomes, activate autoimmune nucleosome‐specific T cells. As these cells may be naïve, such observations do not show that anergic T cells are reactivated. To understand the regulation of autoimmunity, this is important to assess, and this is the focus of this study. T‐Cell anergy was induced by antigen stimulation in the presence of antibodies to the costimulatory molecules CD80/CD86. Requirements for the reactivation of anergic T cells were analysed by the ability of antigen and interleukin‐2 (IL‐2) or IL‐15 to increase T‐cell proliferation and IL‐2 transcription. Data demonstrate that stimulation of T cells with T‐antigen and anti‐CD80/86 antibodies promotes long‐lasting clonal T‐cell anergy. While T‐antigen did not reactivate anergic T cells, proliferation and upregulation of IL‐2 gene transcription was initiated by stimulation with antigen, costimulation and IL‐2 added to the cultures. Proliferation per se was not sufficient to promote the reactivation of anergic T cells, as both IL‐2 and IL‐15 induced proliferation, while antigen and IL‐2, but not IL‐15, upregulated IL‐2 mRNA levels. These data demonstrate that the innate immune system and IL‐2 are central to the initiation and termination of T‐cell anergy.
Antigen‐Specific In Vitro Suppression of Murine Helicobacter pylori‐Reactive Immunopathological T Cells by CD4+CD25+ Regulatory T Cells
Authors: Raghavan S. , Suri‐Payer E. , Holmgren J. 
Published: July 2004

AbstractA Helicobacter pylori‐specific in vitro coculture system was established and used to study the role of CD4+CD25+ regulatory T cells (Treg) in gastritis development in mice with H. pylori infection. Effects of therapeutic immunization against H. pylori infection on the Treg function were also studied to better understand the mechanisms leading to postimmunization gastritis in these mice. Depletion of Treg led to extensive proliferation to H. pylori antigens of CD4+ T cells isolated from either naïve, H. pylori‐infected or H. pylori‐immunized mice. Using the Treg‐depleted CD4+ T cells from immunized mice as effector cells, we compared the suppressive efficacy of Treg isolated from naïve, infected or immunized mice and found that Treg from naïve mice, and slightly less efficiently from infected mice, suppressed the CD25– effector T‐cell response and in most cases were distinctly more efficacious than Treg isolated from immunized mice. The suppressive efficacy of Treg isolated from the differently treated mice correlated closely with production of interleukin‐5 (IL‐5) by the Treg and suppression of interferon‐γ and IL‐2 production by the CD25– effector T cells. Our study is the first to demonstrate in H. pylori‐induced chronic infection, antigen‐specific Treg with differential efficacy in suppressing H. pylori proinflammatory T effector cells.
Monocytes Stimulated with Group B Streptococci or Interferons Release Tumour Necrosis Factor‐Related Apoptosis‐Inducing Ligand
Authors: Halaas Ø. , Liabakk N.‐B. , Vik R. , Beninati C. , Henneke P. , Sundan A. , Espevik T. 
Published: July 2004

AbstractTumour necrosis factor (TNF)‐related apoptosis‐inducing ligand (TRAIL) is a cytotoxic member of the TNF family. Some reports have shown that TRAIL is released from cells in a soluble form. In this work, we have investigated the mechanism of release of TRAIL from monocytes. First, we show that whole gram‐positive, gram‐negative and mycoplasmal bacteria as well as lipopolysaccharide (LPS), interferon‐α (IFN‐α), ‐β and ‐γ all induced upregulation of TRAIL on the surface of human monocytes. Next, we show that IFN‐α, ‐β and ‐γ all induced a dose‐dependent release of TRAIL, giving significant amounts of soluble TRAIL after 2 days. Of the bacteria, only the Group B streptococcus COH‐1 (GBS) induced release of TRAIL and concomittantly induced IFN‐α. Monocytes stimulated with GBS or IFN‐α also showed extensive cell death. When monocyte apoptosis was prevented by interleukin‐1, GM‐CSF, LPS or the caspase inhibitor zVADfmk, the IFN‐α‐induced release of TRAIL was reduced, whereas agents inducing necrosis caused increased release of TRAIL. LPS also prevented release of TRAIL from GBS‐stimulated monocytes. The release of TRAIL from IFN‐α‐stimulated monocytes was reduced by inhibitors of both cysteine and metalloproteases. We conclude that bacteria and IFN induce upregulation of membrane TRAIL and that release of TRAIL is associated with cell death.
If the ‘Adaptive’ Immune System Can Recognize a Significant Portion of the Pathogenic Universe to Which the ‘Innate’ Immune System is Blind, Then…
Authors: Cohn M. 
Published: July 2004

AbstractThe ‘adaptive’ immune repertoire functionally recognizes pathogens (and their toxic products) that the ‘innate’ defense system misses. This requires that the self–nonself discrimination and the regulation of effector output be dependent primarily on somatic learning mechanisms (i.e. on the somatically generated, large, random ‘adaptive’ immune paratopes repertoire).
Characterization of Ribosomal P Autoantibodies in Relation to Cell Destruction and Autoimmune Disease
Authors: Ersvær E. , Bertelsen L.‐T. , Espenes L. C. , Bredholt T. , Bøe S. O. , Iversen B. M. , Bruserud Ø. , Ulvestad E. , Gjertsen B. T. 
Published: July 2004

AbstractAutoantibodies against the ribosomal P proteins are related to cell death and tissue destruction and are frequently exhibited in patients with systemic lupus erythematosus (SLE). In an attempt to explore the effect of tissue destruction on the induction of anti‐P autoantibodies, we searched for anti‐P autoantibodies by enzyme‐linked immunosorbent assay in 201 antinuclear antibody (ANA)‐positive individuals, in 10 patients with treated kidney SLE and in 45 acute leukaemia patients undergoing intensive chemotherapy. The autoantibody reactivity was further characterized using one‐ and two‐dimensional immunoblot analysis and immunofluorescence. Anti‐P were detected in 5.5% (11/201) of ANA‐positive individuals, but not in kidney‐affected SLE patients or in patients with leukaemia. Seven of 11 anti‐P‐positive patients had SLE (3/11), primary Sjögrens's syndrome (1/11) and other autoimmune diseases (3/11). A relation between disease activity and anti‐P was suggested by follow‐up examinations in one SLE patient, supported by the absence of anti‐P autoantibodies in the 10 treated kidney SLE patients. Anti‐P autoantibodies were detected by immunoblot in one patient with SLE indicating anti‐P2 predominance and in the patient with Sjögrens's syndrome indicating anti‐P1 predominance. Diverging humoral responses in these ANA‐ and anti‐P‐positive patients were further illustrated by immunofluorescence, elucidating varying nuclear reactivity and anti‐P pattern. The observation of anti‐P in individuals with active autoimmune disease, but not in patients with chemotherapy‐induced cell damage, suggests that anti‐P antibodies are part of a specific disease process, and not elicited as a response to cell destruction per se.
Response to Cohn: The Immune System Rejects the Harmful, Protects the Useful and Neglects the Rest of Microorganisms
Authors: Dembic Z. 
Published: July 2004

SummaryThe immune system is seen as a guardian of tissue integrity. It would analyse the extent and quality of damage and respond adequately. If no ill effects were found, the system would ignore disturbance, but if beneficial effects were found, it could protect certain microorganisms (establishing commensalism), perhaps via regulatory cells. The Integrity hypothesis proposes three basic groups of intercellular signals for cells of all tissues and assumes that they govern communication between dendritic cells, T cells and B cells. Signal‐1 would be the main information source resulting with generation of intracellular mediators that are bound to travel into the nucleus to achieve reaction. Signal‐2 represents the generation of additional signal transducers representing a modifier at the level of cytosol. And, signal‐3 would be a modifier at nuclear level, perhaps guarding accessibility to chromosome or genetic locus.
Citrullination of Self‐Proteins and Autoimmunity
Authors: Rubin B. , Sønderstrup G. 
Published: July 2004

AbstractCitrullination (deimination is an enzymatic, posttranslational conversion of arginine residues to citrulline residues) of joint‐associated self‐proteins may be a possible mechanism in the induction of autoimmune CD4 T‐cell responses in rheumatoid arthritis. We have studied the immune response to normal or deiminated human fibrinogen (hFBG) in mouse strains expressing major histocompatibility complex (MHC) class II antigens similar to either RA‐susceptible or non‐susceptible HLA‐DR4 alleles. Upon immunization with deiminated hFBG, all mouse strains analysed produced high amounts of anti‐FBG antibodies, while relatively low levels of anti‐citrulline antibodies and little or no anti‐FBG antibodies crossreactive with mouse FBG (mFBG) were obtained. Mice immunized with normal hFBG also produced high amounts of anti‐hFBG antibodies. However, whereas mice with MHC class II molecules similar to RA‐non‐susceptible HLA‐DR4 alleles produced low levels of anti‐hFBG antibodies with crossreactivity to mFBG, mouse strains with RA‐susceptible HLA‐DR4‐equivalent MHC class II molecules contained high levels of such crossreactive anti‐mFBG antibodies. Similar results were obtained with HLA‐DR4*0401, human CD4‐double‐transgenic mice. However, none of the more than 600 mice investigated developed arthritis. These data indicate that the quality and/or quantity of anti‐FBG autoantibodies or of anti‐citrulline antibodies, produced in the studied mouse strains, are insufficient to induce arthritis.
Defective Clearance of Adenovirus in IRF‐1–/– Mice Associated with Defects in NK and T Cells but not Macrophages
Authors: Xu X. , Zhang H.‐G. , Liu Z.‐Y. , Wu Q. , Yang P.‐A. , Sun S.‐H. , Chen J. , Hsu H.‐C. , Mountz J. D. 
Published: July 2004

AbstractA replication‐defective adenovirus‐LacZ recombinant virus (AdLacZ) was injected intravenously into IRF‐1–/– mice and wild‐type mice to characterize the contribution of IRF‐1 to the immune‐mediated clearance of Ad vector. Compared with wild‐type mice, IRF‐1–/– mice expressed higher levels of the LacZ gene product in the liver. After infusion of the AdLacZ, the expression of IRF‐1 mRNA was upregulated in the liver of wild‐type mice, but not in IRF‐1–/– mice. Both spleen and liver mononuclear cells from IRF‐1–/– mice initially exhibited a markedly lower number of NK, NK‐T and CD8 T cells. At day 7 after the administration of AdLacZ, there was a significantly increased population of NK, NK‐T and CD8 T cells in both spleen and liver, and also CD11b+ cells in liver of IRF‐1–/– mice, compared with the increased in wild‐type mice. As IRF‐1 is an important signal for production of IFN‐γ by CD8 T and NK cells as well as production of IL‐12 by CD11b+ cells, we determined whether there were lower levels of these cytokines in IRF‐1–/– mice after Ad challenge. Surprisingly, there were lower levels of IL‐12, but higher levels of IFN‐γ and IL‐18 in IRF‐1–/– compared with wild‐type mice at day 7 after administration with AdLacZ. These results indicate that delayed clearance of Ad is associated with partial correction of defects of the NK, NK‐T and CD8 T cells and increased production of IFN‐γ and IL‐18 in IRF‐1–/– mice.
Current Gene‐Mapping Strategies in Experimental Models of Multiple Sclerosis
Authors: Becanovic K. , Jagodic M. , Wallström E. , Olsson T. 
Published: July 2004

AbstractBoth family‐based linkage analyses and population‐based association studies have failed to identify disease‐regulatory non‐human leucocyte antigen genes of importance in multiple sclerosis (MS). Instead, investigators have employed experimental models, which offer major advantages in genetic studies. We summarize the current main methodologies used and the status of both the human and experimental approaches. Why is it important to find genes regulating MS? There is an immense number of cellular and molecular interactions defined in the immunological field and it is very difficult to unravel those that are critical to an inflammatory disease, such as MS, by classical hypothesis‐driven research. Unbiased genetics defines evolutionary conserved gene polymorphisms and pathways regulated by these genes, which are central in the pathogenesis. These, in turn, are of interest as therapeutic targets and pharmacogenetic markers.