bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monoclonal antibodies raised against engineered soluble mouse T cell receptors and specific for Vα8‐, Vβ2‐ or Vβ10‐bearing T cells
Authors: Necker Antje , Rebaï Najet , Matthes Michaela , Jouvin‐Marche Evelyne , Cazenave Pierre‐André , Swarnworawong Pam , Palmer Ed , Robson MacDonald H. , Malissen Bernard 
Published: March 2007

AbstractWe have characterized a panel of monoclonal antibodies (mAb) produced by immunizing rats with two distinct soluble mouse α/β T cell receptor (TcR). Fifty mAb were found to react with the corresponding surface‐bound TcR. Such observations suggest that the soluble TcR molecules used as immunogen are folded in a conformation similar to the native structure. Furthermore, the binding to T cells of four antibodies was found to correlate with the expression of the Vα8, Vβ2 or Vβ10 gene segments. Finally, staining of T lymphocytes from various mouse strains suggests that (a) the two anti‐Vα8 antibodies recognize different epitopes, and each on only a fraction of Vα8+ cells; (b) the anti‐Vβ10 mAb identifies a Vβ10 polymorphism among mouse strains, and (c) T cells expressing the Vβ2 or Vβ10 gene segments are not subject to major clonal deletion events induced by the major histocompatibility complex class II and Mls products which were tested.
Is early repopulation of macrophage‐depleted lymph node independent of blood monocyte immigration?
Authors: Mebius Reina E. , Martens Gratia , Brevé John , Delemarre Frans G. A. , Kraal Georg 
Published: March 2007

AbstractPopliteal lymph nodes (LN) of mice were depleted of their macrophage (Mϕ) populations in the subcapsular sinus and medulla by subcutaneous injection of dichloromethylene diphosphonate (Cl2MDP)‐containing liposomes into the footpads. Complete restoration of both Mϕ populations could be observed as late as 5 months after liposome administration. This relatively long repopulation time could be due to a depot of liposomes, directly killing all Mϕ precursors after extravasation into the interstitial tissue of the footpad. On the other hand, local interstitial precursors with very low turnover rates may have been depleted in the interstitial tissue of the hind leg. Therefore, two different types of experiments were performed; one in which Mϕ‐depleted LN were replaced by control LN at various time points after liposome treatment, and another whereby Mϕ‐depleted LN were transplanted into control animals.When liposome‐treated, Mϕ‐depleted LN were transplanted into control animals, a complete restoration of both populations in the subcapsular sinus and medulla could be observed within 5 weeks. Control LN transplanted into a Cl2MDP‐liposome‐treated leg showed a rapid disappearance of Mϕ from the subcapsular sinus and medulla and these cell populations remained absent for at least 7–8 weeks after liposome treatment, when the first cells started to reappear. Complete repopulation of these areas by Mϕ took as long as 15 weeks. Using labeled liposomes the presence of a continuous liposome depot was found to be very unlikely.These results suggest that the population of precursor cells that will give rise to Mϕ in the subcapsular sinus and medulla of a LN is probably contained within the interstitial tissue and is almost independent of precursor supply from the blood compartment.
The ligand recognized by ELAM‐1 on HL60 cells is not carried by N‐linked oligosaccharides
Authors: Leeuwenberg Jet F. M. , Tan Agnes , Jeunhomme Trudi M. A. A. , Ploegh Hidde L. , Buurman Wim A. 
Published: March 2007

AbstractThe sialyl Lewis‐x determinant is a ligand for ELAM‐1, a major adhesion molecule for HL60 cells and neutrophils. ELAM‐1 expression can selectively be induced on human umbilical vein endothelial cells (HUVEC) by tumor necrosis factor, interleukin 1 and lipopolysaccharide. The determinant sialyl Lewis‐x is found on both glycolipids as well as on glycoproteins. Using specific inhibitors of the biosynthesis of N‐linked glycosylated glycoproteins, we investigated whether N‐linked glycans or their modifications are involved in ELAM‐1‐dependent adhesion of HL60 cells to activated HUVEC. The inhibitors of glycoprotein processing N‐methyl‐deoxynojirimycin, 1‐deoxymannojirimycin and swainsonine did not affect ELAM‐1‐dependent adhesion. Complex‐type N‐linked glycans are not required for ELAM‐1‐mediated adhesion, and therefore the ligand for ELAM‐1 is most likely a glycolipid, or a glycoprotein carrying O‐linked oligosaccharides.
Internalization of glycosyl‐phosphatidylinositol (GPI)‐anchored lymphocyte proteins II. GPI‐anchored and transmembrane molecules internalize through distinct pathways
Authors: Bamezai Anil , Goldmacher Victor S. , Rock Kenneth L. 
Published: March 2007

AbstractLy‐6A.2 (T cell‐activating protein, TAP) and Thy‐1 are glycosyl‐phosphatidylinositol (GPI)‐anchored proteins expressed on the surface of murine T lymphocytes. We have found that Ly‐6A.2 (TAP) and Thy‐1 are internalized by T cells. In the present study we have investigated whether these GPI‐anchored proteins enter cells by endocytosis through coated pits. Two lines of evidence argue against the involvement of coated pits in the internalization of Ly‐6A.2 (TAP) and Thy‐1. First, drugs that effectively blocked the endocytosis of transferrin receptor and H‐2 class I molecules, (which are known to be internalized via coated pits) did not inhibit the internalization of the GPI‐anchored proteins. Second, in ultrastructural analyses, Ly‐6A2 (TAP) and Thy‐1, in contrast to the transferrin receptor, were rarely found in coated pits or vesicles. These observations suggest that the GPI‐anchored proteins on T lymphocytes are internalized by a distinct pathway that does not involve endocytosis through coated pits.
Specificity and T cell receptor β chain usage of a human collagen type II‐reactive T cell clone derived from a healthy individual
Authors: Yan Tan , Burkhardt Harald , Ritter Thomas , Bröker Barbara , Mann Karl Heinz , Bertling Wolf M. , Mark Klaus Von Der , Emmrich Frank 
Published: March 2007

AbstractCollagen type II (CII) is a cartilage‐specific matrix compound well known as an inducer of an experimental. T cell‐dependent autoimmune arthritis, a disease which shows some similarities to human rheumatoid arthritis. Here we report on an HLA‐DR7‐restricted human CD4 T cell clone (TC9), which was isolated from a healthy donor and recognizes human CII. After screening CNBr fragments of CII and tryptic fragments derived thereof, the T cell epitope could be mapped to amino acid residues 271‐285 of the triple helical region of CII that are located within CNBr fragment 11 [α1 (II) CB11]. This epitope was confirmed by a synthetic peptide stimulatory for TC9. The T cell receptor β chain of TC9 was cloned using the polymerase chain reaction; it comprises Vβ6.7 and contains besides Jβ2.3 and Cβ2 an as yet undescribed sequence for the D segment.
Genetic correction of cultured T cells from an adenosine deaminase‐deficient patient: Characteristics of non‐transduced and transduced T cells
Authors: Braakman Eric , Van Beusechem Victor W. , Van Krimpen Brigitte A. , Fischer Alain , Bolhuis Reinder L. H. , Valerio Dinko 
Published: March 2007

AbstractT lymphocytes derived from peripheral blood of a patient with adenosine deaminase (ADA) deficiency were expanded in vitro. The human ADA (hADA) gene was introduced into these replicating ADA− T cells with the use of an amphotropic recombinant retrovirus carrying the hADA gene. Subsequently, infected T cells were selected on the basis of their ADA expression, by exposure to a combination of the toxic agent xylofuranosyl‐adenine and the specific ADA inhibitor 2′‐deoxycoformycin. CD4+ and CD8+ T cells could be infected and selected with equal efficiencies. The genetically modified T cells were shown to contain intact copies of the provirus and to express normal levels of hADA. As expected, uninfected T cells from the ADA‐deficient patient displayed an increased sensitivity to 2′‐deoxyadenosine. Following genetic modification, however, this sensitivity was restored to normal levels in both CD4+ and CD8+ T cells. The introduction of the hADA gene into the genome of the in vitro expanded T cells did not alter their phenotype, proliferative capacity or cytotoxic potential. These characteristics were identical to those of T cells derived from healthy individuals. These findings are of critical importance for the clinical application of hADA gene‐transducted T cells.
Thymic nurse cell lymphocytes react against self major histocompatibility complex
Authors: Penninger Josef , Wick Georg 
Published: March 2007

AbstractIt has been postulated that thymic nurse cells (TNC), lymphoid‐epithelial complexes composed of thymocytes enclosed within major histocompatibility complex (MHC) class I+ and class II+ cortical epithelial cells, may provide an optimal microenvironment for the process of T cell selection. By transplanting single TNC in the avian chorionallantoic membrane assay we demonstrate that a significant portion of intra‐TNC lymphocytes (TNC‐L) possess reactivity against self‐MHC molecules. The frequency of these autoreactive cells among TNC‐L exceeds by far that of thymocytes or peripheral blood lymphocytes of the same donor. These results indicate that TNC‐L constitute a T cell population enriched for self‐MHC reactivity, i.e. cells that have undergone positive selection, but not yet deletion and/or deactivation.
Novel excision products of T cell receptor γ gene rearrangements and developmental stage specificity implied by the frequency of nucleotide insertions at signal joints
Authors: Iwasato Takuji , Yamagishi Hideo 
Published: March 2007

AbstractWe have cloned circular DNA excised by T cell receptor (TcR)γ1, γ2 and γ3 gene rearrangements in fetal and adult mouse thymocytes. Circular DNA contained a signal joint reciprocal to the genomic V‐J coding joint. Although signal joints without nucleotide insertions are common in immunoglobulin (Ig) and TcR gene rearrangements, the signal joint of γ found in adult thymocytes contained non‐germ‐line element (N) insertions at high frequency, while no insertions were found in fetal thymocytes. Thus developmental stage specificity of TcR γ gene rearrangements is faithfully reflected on the signal joint of excision products. In addition, examination of γ gene excision products revealed circular DNA products of TcR γ‐α transrearrangements, but no evidence for Vγ gene replacement in a rearranged segment.
Studies on the induction of anterior chamber‐associated immune deviation (ACAID) III. Induction of ACAID depends upon intraocular transforming growth factor‐β
Authors: Wilbanks Garth A. , Mammolenti Michele , Streilein J. Wayne 
Published: March 2007

AbstractDelayed hypersensitivity (DH), the prototypical form of cell‐mediated immune responsiveness, is mediated with the participation of considerable nonspecific inflammation which necessarily disrupts the anatomic integrity of involved and adjacent tissues. Damage of this type is of minor consequence to many visceral and cutaneous organs, but is of devastating consequence for organs such as the eye and the brain. At least in the case of the eye, the organ is remarkably adept at regulating the immune system's ability to respond to intraocular antigens by selectively down‐regulating both the induction and expression of delayed hypersensitivity while leaving other effector modalities intact. This ability of the eye to selectivity down‐regulate systemic DH responses to intracamerally inoculated antigens is known as anterior chamber‐associated immune deviation (ACAID) and is mediated in part by antigen‐specific regulatory T cells. Recent work suggests that macrophages (MΦ) that reside in the iris and ciliary body can migrate out of an antigen‐bearing eye and activate regulatory T cells within the spleen. In an effort to understand the mechanism by which intraocular MΦ interact with antigen in the anterior chamber of the eye (AC) and subsequently induce splenic regulatory cells in ACAID, we have investigated what role, if any, the AC microenvironment itself plays in ACAID induction. The results reveal that CD45− parenchymal iris/ciliary cells secrete a soluble factor(s) locally and into the aqueous humor which endows resident, mature MΦ with ACAID‐inducing capabilities. Mice receiving infusions of these altered, antigen‐pulsed MΦ are incapable of mounting a significant DH response following immunization with antigen in adjuvant. Importantly, the ACAID‐inducing effect is achieved when conventional, extraocular MΦ are exposed in vitro to a soluble factor present in aqueous humor or culture SN from iris and ciliary body cells. Further investigations into the identity of this factor reveal it to be transforming growth factor‐β (TGF‐β). The role of TGF‐β in the generation of ACAID, as well as the implications of these findings to an understanding of immunologic privilege in general, are discussed.
Augmentation of major histocompatibility complex class I and ICAM‐1 expression on glial cells following measles virus infection: Evidence for the role of type‐1 interferon
Authors: Kraus Elmar , Schneider‐Schaulies Sibylle , Miyasaka Masayuki , Tamatani Takuya , Sedgwick Jonathon 
Published: March 2007

AbstractAn intracellular staining procedure for the cytoskeletal marker, glial fibrillary acidic protein of astrocytes, has been developed which allows flow cytometric phenotyping of astrocytes within complex mixtures of glial cells. Employing this technique, we show here that measles virus infection of rat mixed glial cell cultures results in a rapid augmentation of major histocompatibility complex (MHC) class I and ICAM‐1 on the majority of astrocytes in culture. MHC class I levels are increased on macrophages/microglia but ICAM‐1 expression is not normally affected on this cell type. Some MHC class II induction is also observed after virus infection but only on astrocytes. A type‐I interferon (IFN)‐inducible protein, Mx, was identified in cultured glial cells after infection. Qualitatively comparable MHC class I and ICAM‐1 enhancement after addition of type‐I IFN, supports the conclusion that this cytokine(s) released as a result of virus infection, is responsible for alterations in the expression of molecules on glial cells, that are involved in T cell recognition. Astrocytes after viral infection were more susceptible to alloantigen‐specific cytotoxic T lymphocytes and cytotoxic T lymphocyte activity was substantially reduced in the presence of mAb specific for MHC class I, ICAM‐1 and LFA‐1 but not MHC class II. The relevance of these findings to T cell recognition of virus‐infected cells in the central nervous system is discussed.
Acute human vs. mouse graft vs. host disease in normal and immunodeficient mice
Authors: Huppes Wim , Geus Bernard De , Zurcher Chris , Van Bekkum Dirk W. 
Published: March 2007

AbstractRecent reports of persistent engraftment of human lymphocytes and myeloid cells in hereditary immunodeficient severe combined immunodeficient mice (SCID) and beige athymic nude X‐linked immunodeficiency (Bg/Nu/XID) mice have raised the question of why attempts to graft human cells into artificially immunosuppressed normal mice have failed so far. In the present study we provide evidence that this difference is due to the absence of natural antibodies in the mutant mice. We demonstrate that human PBL can be grafted in normal mice immunosuppressed by heavy doses of total body irradiation, provided the transplant is performed when the recipients lack natural antibodies in their serum, e.g. as in newborn normal mice, in mice treated with anti‐mouse IgM antibody from birth, and in 3‐week‐old B cell‐deficient CBA/N mice. In all cases, large numbers of human PBL were required.Under these conditions an acute and fatal graft vs. host disease (GVHD) developed in the recipients, regardless of whether these were artificially immunosuppressed or hereditary immunodeficient. The clinical manifestations and the histopathology of this xenogeneic acute GVHD are quite different from those of allogeneic GVHD. The former is primarily confined to the hematolymphoid tissues and locations close to accumulations of proliferating lymphoblasts, such as the peritoneal cavity in case of i.p. transplantation. The discordant xenogeneic GVHD is induced by human T lymphocytes and can be abrogated by treatment with anti‐human T cell serum.
Tolerance of self induced in thymus organ culture
Authors: Robertson Katherine , Simon Katharina , Schneider Susanne , Timms Emma , Mitchison Avrion 
Published: March 2007

AbstractF liver protein occurs in serum at low concentration, and therefore induces tolerance of self only in T cells. T cells which mature in cultured thymus lobes in the absence of this protein become reactive towards it but can be prevented from doing so by exposure to the protein while in culture. The threshold of tolerance induction for this soluble antigen is estimated in this way at ∼ 1 μg/ml, which is slightly less than the threshold of response of primed T cells in a proliferation assay. Freshly isolated thymocytes do not display reactivity to self‐F protein, indicating that T cells normally become tolerant while still within the thymus.
Induction of experimental autoimmune encephalomyelitis by native myelin basic protein‐activated T lymphocyte lines
Authors: Friedman Aharon , Reshef Tamara , Cohen Irun R. 
Published: March 2007

AbstractSelf antigens bind to MHC class II molecules in vivo. The capacity of class II molecules to bind native self antigen, namely antigen that has not been processed through an endososomal pathway, could increase susceptibility to autoimmune diseases if recognized by autoreactive T lymphocytes. To confirm this prediction we designed experiments to show that: (a) native myelin basic protein (BP) activates encephalitogenic T lymphocyte lines, and (b) these activated lines cause experimental autoimmune encephalomyelitis (EAE) in naive rats. We show that two encephalitogenic T lymphocytes lines, LEW and BN, are activated by native BP in the presence of paraformaldehyde pre‐fixed antigen‐presenting cells (APC). The degree of activation, as measured by T lymphocyte proliferation, was equal to that obtained in response to BP processed by APC prior to paraformaldehyde fixing. The response to native BP was confirmed by demonstrating insensitivity to the presence of the lysosomotropic agent chloroquine or protease inhibitors. Activation of T lymphocytes by BP required the presence of syngeneic APC. The activated T lymphocyte lines were injected into naive recipient rats that developed EAE within 5 days. Both disease incidence and severity were equal to that observed in rats that were treated with T lymphocytes activated by processed BP. Hence, at least in EAE, the risk of an autoimmune event could be precipitated by a complex of native antigen and class II molecules on cells that do not possess an endososomal pathway for antigen processing and presentation.
Hierarchy of responsiveness in vivo and in vitro among T cells expressing distinct MIs‐1a‐reactive Vβ domains
Authors: Waanders Gary A. , McDonald H. Robson 
Published: March 2007

AbstractIn this report we have compared responses of T cells bearing different T cell receptor (TcR) Vβ domains, including Vβ6, 7, 8.1 and 9, to the minor lymphocyte stimulatory locus (MIs‐1a). The virtually complete deletion of peripheral T cells using these TcR Vβ domains in mice expressing MIs‐1a verified their MIs‐1a reactivity. However, varied responses among these cells following stimulation with MIs‐1a in vitro suggested a hierarchy of TcR reactivities for MIs‐1a with Vβ6 and Vβ9 > Vβ8.1 » Vβ7. This hierarchy was further supported by in vivo studies which showed that Vβ6+CD4+ cells dominated responses to MIs‐1a.
Phenotype, activation and lymphokine secretion by γ/δ T lymphocytes from schistosomiasis and carcinoma of the urinary bladder
Authors: Raziuddin Syed , Shetty Sugandh , Ibrahim Ahmed 
Published: March 2007

AbstractIn humans the majority of the CD3+ T cells usually express an α/ß T cell receptor (TcR) and a minority express a γ/δ TcR. The CD3+ TcR α/ß and CD3+ TcR γ/δ cells from blood of the patients with schistosomiasis with carcinoma of the urinary bladder (SCB) were analyzed for phenotype, activation, secretion of interleukin 2 (IL2), B cell growth factor (BCGF) and B cell differentiation factor (BCGF), as well as for autologous (AMLR) and allogeneic (MLR) mixed lymphocyte reaction. Patients with SCB had a highly increased percentage of CD3+ TcRγ/δ and a decreased percentage of CD3+ TcR γ/ß T cells in their circulation. These CD3+ TcR γ/δ T cells expressed the CD25 (IL 2 receptor), CD38, CD71 (transferrin receptor) and HLA‐DR activation antigens at a higher intensity after in vitro stimulation with recombinant IL 2, phytohemagglutinin and soluble egg antigen (from Schistosoma haematobium). The SCB patients' CD3+ TcR γ/δ T cells were highly deficient in secretion of IL 2 but produced highly elevated levels of BCGF and BCDF. On the contrary, both BCGF and BCDF activities of the CD3+ TcR α/β T cells were decreased. Moreover, CD3+ TcR γ/δ T cells demonstrated highly deficient AMLR and MLR activity. These observations suggest a possible role of CD3+ TcR γ/δ T cells in the immune response and the disease pathogenesis in human schistosomiasis infections.
Increased frequency of 2,4,6‐trinitrophenyl (TNP)‐specific, H‐2b‐restricted cytotoxic T lymphocyte precursors in transgenic mice expressing a T cell receptor β chain gene from an H‐2b‐restricted, TNP‐specific cytolytic T cell clone
Authors: Iglesias Antonio , Hansen‐Hagge Thomas , von Bonin Arne , Weltzien Hans Ulrich 
Published: March 2007

AbstractT cell antigen receptors (TcR) expressing Vα10/JαBBM142 genes in association with β chains containing Jβ2.6 elements were found to be predominant among 2,4,6‐trinitrophenyl (TNP)‐specific, H‐2b‐restricted cytolytic T cell lines (CTL). To assess the relative contribution of the TcR β chain to the TNP specificity as well as to the selection of the respective TcR α chain elements we generated transgenic mice expressing the TcR β chain of the H‐2b/TNP‐specific CTL clone BT7.4.1. The TcR of this clone does not belong to the type predominant among H‐2b/TNP‐specific CTL, as it consists of an α chain encoded by a Vα8/JαDO gene rearrangement and a Vβ2/Jβ1.1‐containing β chain. In the transgenic mice almost all T cells exclusively express the transgenic Vβ2 gene, as a result of allelic exclusion. TNP‐specific, H‐2b‐restricted precursors were found at 7‐ to 8‐fold higher frequency in these mice as compared with non‐trangenic littermates. In H‐2b/d heterozygous transgenic mice, an increased frequency of TNP‐specific precursors was found only in H‐2b, but not in H‐2d‐restricted CTL. Analysis of H‐2b/TNP‐specific CTL lines derived from Vβ2‐transgenic mice indicated a preferential association of the transgenic TcR β chain with endogenous α chains encoded by Vα8 and JαBBM142 genes. This suggests that the hapten TNP is recognized like typical peptide antigens by combinatorial TcR α and β contact sites.