bluuebunny/crossref_metadata_2025_split huggingface dataset:
Restricted expression of T cell receptor Vβ but not Vα genes in rheumatoid arthritis
Authors: Sottini Alessandra , Imberti Luisa , Gorla Roberto , Cattaneo Roberto , Primi Daniele 
Published: March 2007

AbstractSynovial fluids of patients with rheumatoid arthritis contain activated T lymphocytes that may play an important role in the pathogenesis of the disease. Previous studies have suggested that the T cell receptor (TcR) repertoire of these cells is restricted, reflecting in vivo selection of a limited number of T cell specificities at the site of inflammation. To characterize better these T cell populations we used the polymerase chain reaction technology to estimate the proportion of TcR α and β RNA containing any particular V elements from transcripts directly isolated from the synovial fluid cells and from peripheral blood mononuclear cells of three patients with rheumatoid arthritis. Our data show that, in contrast to peripheral blood mononuclear cells, synovial fluid T cells expressed only few Vβ transcripts, one of which was overrepresented in two patients. Peripheral and joint fluid T cells, on the other hand, appeared to express the same set of non‐restricted Vα elements. These results suggest that a major antigen associated with the pathogenesis of rheumatoid arthritis may interact selectively with the Vβ component of the TcR.
A single‐chain murine class I major transplantation antigen
Authors: Mottez Estelle , Jaulin Christian , Godeau François , Choppin Jeanine , Levy Jean‐Paul , Kourilsky Philippe 
Published: March 2007

AbstractSingle‐chain mouse Kd molecules (SC‐Kd) were engineered by connecting residue 276 of Kd heavy chain to the first residue of β2‐microglobulin through spacers of various lengths, and expressed intracellularly in monkey COS‐1 cells. Labeled SC‐Kd molecules were found to react with several monoclonal antibodies which recognize native Kd molecules. SC‐Kd‐15 (with a spacer of 15 residues) was studied in more details. It could be purified and shown to regain a native‐like structure after treatment with denaturing agents. Purified SC‐Kd‐15 could bind certain peptides in a manner qualitatively similar to that of Kd.
Cytotoxicity and immunocyte markers in cells from the freshwater snail Planorbarius corneus (L.) (Gastropoda pulmonata): implications for the evolution of natural killer cells
Authors: Franceschi Claudio , Cossarizza Andrea , Monti Daniela , Ottaviani Enzo 
Published: March 2007

AbstractThe hypothesis that natural killer (NK) cells represent an important form of cell recognition and cytotoxicity leads to the prediction that NK‐like activity should be preserved throughout phylogenetic development. This was tested in the invertebrate Planorbarius corneus. Two types of cells can be identified and separated from the hemolymph of this mollusc, i.e. glass‐adherent macrophage‐like spreading hemocytes (SH) and nonadherent round hemocytes (RH). Only RH are able to lyse the K‐562 human target cell line in a short‐term NK cytotoxicity test. This NK‐like activity, severely reduced after 18 h incubation at 24 °C, is preserved by human recombinant interleukin 2. A further analysis of P. corneus hemocytes has been performed by using several mouse anti‐human monoclonal antibodies and cytofluorimetric analysis. Unexpectedly, both SH and RH react with several monoclonal antibodies, including those directed against epitopes typical of mammalian NK cells and cell adhesion molecules. On the whole, these data support the hypothesis that a primitive NK‐like activity appeared early in evolution and is not shared by phagocytic cells.
β1 Integrin‐mediated lymphocyte adherence to extracellular matrix is enhanced by phorbol ester treatment
Authors: Wilkins John A. , Stupack Dwayne , Stewart Steve , Caixia Shen 
Published: March 2007

AbstractThe interaction of the human T cell leukemia, Jurkat, with the extracellular matrix components collagen and fibronectin was examined. These cells displayed constitutive binding to fibronectin and low levels of adherence to collagen which were enhanced following stimulation with phorbol esters. The relevant binding structures were identified as members of the CD29/β1 integrin family of adhesion molecules. Adherence to collagen and to fibronectin was mediated by α2β1 and α5β1, respectively. The enhancement of adherence by phorbol esters did not involve up‐regulation of receptor expression but appeared to derive from the increased functionality of structures which were expressed on the cell surface.
Modulation of type II Fcγ receptor expression on activated human B lymphocytes
Authors: Sármay Gabriella , Rozsnyay Zoltán , Szabó Ildikó , Biró Anna , Gergely János 
Published: March 2007

AbstractWe have monitored FcγRII expression during the activation of human B lymphocytes by simultaneous analysis of monoclonal antibody (mAb) binding and EA resetting. The expression of FcγRII showed a biphasic time course. Initially, a transient increase of FcγRII with no ligand‐binding capacity was observed with mAb staining as early as 10 min after stimulation by the F(ab')2 fragment of anti‐human IgM or phorbol 12‐myristate 13‐acetate and then after 3 to 24 h a decrease in the number of FcγRII+ cells was seen. Trypsin‐like serine protease activity also appeared in the lysate of activated B cells at this time. On the 2nd day of activation a significant enhancement of FcγRII expression was observed, mainly on enlarged blast cells as monitored by both mAb and by ligand binding (EA rosette). At the same time, soluble fragments of FcγRII with the ability to bind human Fc were detected in the supernatant of activated B cells, probably as a result of proteolytic cleavage. These findings suggest that activated B cells are identical with the population of mononuclear cells which shed FcγR when incubated at 37°.The ability of activated but not resting B cells to release FcγRII correlates with the expression of early activation markers and with the appearance of a trypsin‐like serine protease activity of the same cells; thus, the release of FcγRII occurs in the early G1 phase of cell cycle as a result of proteolysis. Later the release of FcγRII is accompanied by the enhancement of FcγRII expression before the cells reach the S phase.The fragments of cleaved FcγRII had an apparent molecular mass of 33 and 14–18 kDa under nonreducing conditions, and upon reduction fragments of smaller size were observed.
Interleukin 2/interleukin 4‐independent T helper cell generation during an in vitro antigenic stimulation of mouse spleen cells in the presence of cyclosporin A
Authors: Motta Iris , Colle Jean‐Hervé , Shidani Babak , Truffa‐Bachi Paolo 
Published: March 2007

AbstractCyclosporin A (CsA), an immunosuppressive drug which completely suppresses the humoral response to thymus‐dependent antigens, does not affect the generation of T helper (Th) cells during an in vitro stimulation of murine spleen cells with sheep red blood cells. The appearance of Th cells depends on time and their development can be prevented by X‐ray irradiation performed at the onset of the culture and up to 3–4 days later; however, beyond this time, irradiation is ineffective, suggesting that cell proliferation is essentially completed by this time. The activity of Th cells generated in the presence of CsA is resistant to irradiation, indicating that the effector cells belong to a memory subset. Limiting dilution analysis has shown that the frequency of the Th cells recovered from 6‐day sheep red blood cell‐stimulated and CsA‐treated cultures is of approximately 1.4 × 10−3, representing an increment of about 500‐fold compared to naive spleen cells. The increased frequency of Th cells and the sensitivity to irradiation of the generation of these cells demonstrate that Th cell precursors proliferate in the presence of CsA. Lymphokine genes transcription analysis confirms that the inhibition of interleukin (IL) 2/IL 4 gene expression is one target of CsA action. That the generation of Th memory cells can nevertheless take place strongly argues in favor of the existence of an IL 2/IL 4‐independent pathway for murine T cell proliferation. Our finding that the transcription of the IL 7 gene is not inhibited by CsA raises the possibility for a role of this T cell growth factor in the generation of memory Th cells.
Conserved nucleotide sequences at the 5' end of T cell receptor variable genes facilitate polymerase chain reaction amplification
Authors: Broeren Chris P. M. , van Eden Willem , Kusters Johannes G. , Lenstra Johannes A. , Verjans Georges M. G. M. , Logtenberg Ton 
Published: March 2007

AbstractAlignment of all available nucleotide sequences of mouse and rat α/β T cell receptor (TcR) variable (V) regions revealed the presence of relatively conserved sequences at the 5' end of the V gene segments. Based on these conserved sequences, degenerate primers were developed for use in the polymerase chain reaction (PCR). The degenerate primers developed on the basis of the conserved sequences at the 5' end of rat and mouse V gene segments are expected to enable the amplification of all mouse and rat TcR α/β chain V regions. To test their applicability, the primers were used for the amplification of the V region of the TcR α/β expressed by rat T cell lines. After amplification, the TcR V regions expressed were cloned and sequenced. The Zla T cell line was shown to use the same TcR V gene segments (Va2 and Vβ8.2), as most other experimental allergic encephalomyelitis associated T cell lines, but had different D and J segments. In spite of these differences at the nucleotide level, a remarkable conservation of the amino acid sequence at the VbTDβJβ junction was found.Alignment of a large number of human Vα and Vβ gene segments revealed the presence of similarly conserved sequences. Degenerate primers based on these conserved sequences enabled the amplification of TcR V regions of human T cell lines.
Coding joint formation of endogenous T cell receptor genes in lymphoid cells from scid mice: unusual P‐nucleotide additions in VJ‐coding joints
Authors: Schuler Walter , Amsler Michaela , Ruetsch Norman R. , Bosma Melvin J. 
Published: March 2007

AbstractThe mouse mutation scid adversely affects the process of VDJ recombination. Attempts to form coding joints, that is, to join V or D to J gene segments generally fail in developing scid lymphocytes. It has been proposed that the scid mutation results a defective VDJ recombinase system. Here we describe five scid T cell lymphomas containing one or two TcRγ coding joints each, even though the majority of the multiple TcRγ chain gene rearrangements and all TcRβ rearrangements in these cells were abnormal with the deletions typically found in scid lymphoid cells. One of the five T cell lymphomas was shown to have an active VDJ recombinase system; however, this activity was defective indicating that the scid phenotype has been retained. We conclude that the scid VDJ recombinase system has not completely lost the ability to form coding joints. P‐nucleotide additions of unusual length or composition were found at the junctional border in five of the eight TcRγ coding joints. This might reflect a defect in the activity of a component of the VDJ recombinase system involved in the generation of P‐nucleotide additions. In one of the observed rearrangements, a Vγ5‐Jγ3 coding joint was formed. This establishes the transcriptional orientation of Jγ3‐Cγ3 and confirms a previously proposed organization of the TcRγ genes.
Self‐reactive T cells are activated by the 65‐kDa mycobacterial heat‐shock protein in neonatally thymectomized mice
Authors: Iwasaki Akinori , Yoshikai Yasunobu , Yuuki Hiroyuki , Takimoto Hiroaki , Nomoto Kikuo 
Published: March 2007

AbstractTo elucidate the mechanism of autoimmune disease in neonatally thymectomized (NTX) mice, we have investigated the responsiveness of the self‐reactive T cells which have not undergone clonal deletion in such animals. Consistent with a recent report (Yuuki et al., Eur. J. Immunol. 1990. 20: 1475), T cells bearing Vβ11‐gene products capable of recognizing I‐E‐encoded molecules were readily detected in the mature T cell pool of NTX BALB/c (I‐Ed, Mls‐2a) mice. The Vβ11‐bearing T cells in NTX mice expressed interleukin 2 receptors and responded normally to signals delivered through the T cell receptor. Notably, these T cells in NTX mice proliferated significantly after culture with the 65‐kDa mycobacterial heat‐shock protein, whose amino acid sequence is highly homologous to that in eukaryotes. These results suggest that self‐reactive T cells in NTX mice may be activated by heat‐shock proteins derived from various pathogens and/or stressed autologous cells, resulting in the development of autoimmune diseases in such animals.
Susceptibility to the induction of either autoimmunity or immunosuppression by mercuric chloride is related to the major histocompatibility complex class II haplotype
Authors: Aten Jan , Veninga Aletta , de Heer Emile , Rozing Jan , Nieuwenhuis Paul , Hoedemaeker Philip J. , Weening Jan J. 
Published: March 2007

AbstractMercuric chloride (HgCl2) induces in Brown Norway rats a CD4+ T lymphocyte‐dependent systemic autoimmune syndrome, involving synthesis of anti‐glomerular basement membrane autoantibodies and development of proteinuria. Lewis rats are resistant to HgCl2‐induced autoantibody production and, in contrast, develop immunosuppression, mediated by CD8+ T lymphocytes. In the present study, genetic requirements governing autoreactivity or immunosuppression in response to HgCl2 were further explored. Both major histocompatibility complex (MHC) and non‐MHC genes are involved in determining susceptibility to HgCl2‐induced autoimmunity. Both AO (RT1u) and DZB (RT1u) rats were found to develop a membranous autoimmune glomerulopathy upon exposure to HgCl2. Only the DZB strain, which differs in part of the non‐MHC background from AO, developed proteinuria. AO.1P (RT1.AuBlDlEu) rats, which are genetically identical to AO except for the Lewis haplotype at the MHC class II loci, appeared to develop immunosuppression upon exposure to HgCl2. It is concluded that autoreactivity and immunosuppression, induced by HgCl2, are both dependent on the MHC class II haplotype. In autoimmune responder strains the type of autoimmune glomerulopathy is influenced by non‐MHC genes.
Characterization of the rat leukocyte integrin, CD11/CD18, by the use of LFA‐1 subunit‐specific monoclonal antibodies
Authors: Tamatani Takuya , Kotani Masaharu , Miyasaka Masayuki 
Published: March 2007

AbstractWe have attempted to characterize the rat leukocyte integrin, CD11/CD18, by the use of newly generated monoclonal antibodies (mAb) WT.1 (anti‐CD11a) and WT.3 (anti‐CD18) in conjunction with an mAb, OX42, reactive with a rat integrin‐like molecule, with respect to the biochemistry, cellular distribution and function. The conclusion that the mAb WT.1 and WT.3 specifically recognize the rat CD11a and CD18, respectively, was based on: (a) their ability to inhibit homotypic aggregation of splenic concanavalin A (Con A) blasts; (b) sodium dodecyl sulfate‐polyacrylamide gel electrophoretic analysis of the antigens recognized; (c) their ability to inhibit binding of Con A blasts to the purified ligand, namely the ICAM‐1 antigen and (d) their blocking abilities in mixed leukocyte reaction.In the rat, CD18 has an apparent molecular mass of 95–100 kDa and can associate with at least three distinct α subunits of 160–170 kDa (CD11a), 140–150 kDa and 120–130 kDa. The latter two are precipitated by OX42 from MΦ but not from unstimulated lymphocytes. They presumably represent the rat CD11b and CD11c, respectively. Rat thymocytes, PBL, thoracic duct lymphocytes, monocytes and neutrophils expressed differential levels of CD11a and CD18. Peritoneal MΦ showed virtually no CD11a expression, although CD18 was expressed at levels similar to those seen on blood monocytes, showing an interesting pattern of LFA‐1 expression regulation in this cell lineage. Both WT.1 (anti‐CD11a) and WT.3 (anti‐CD18) apparently recognize a “low‐affinity” as well as a “high‐affinity” form of LFA‐1 and do not discriminate between the two.
Molecular basis of IgG Fc receptor III defect in a patient with systemic lupus erythematosus
Authors: Enenkel Barbara , Jung Dirk , Frey Jürgen 
Published: March 2007

AbstractBy flow cytometry analysis we could show a decreased expression of Fcγ receptor type III (FcγRIII) on granulocytes of a patient with systemic lupus erythematosus (SLE). Therefore, we constructed a leukocyte cDNA library from this patient with the aim of investigating this defect on the molecular level. Using an FcγRIII cDNA probe we isolated 15 FcγRIII cDNA clones, which were all characterized by sequencing. Our sequence data revealed that the patient was heterozygous for FcγRIII (NA‐1/NA‐2). Only clone 5 (NA‐2) was a full‐length cDNA clone. In contrast to the wild‐type FcγRIII the signal sequence is mutated, lacking the hydrophobic region essential for co‐translational transport across the endoplasmic reticulum membrane. The predicted transport defect leading to the lack of membrane expression could be confirmed by immunofluorescence staining after expression of this cDNA clone in BHK cells. The cDNA clones 6 and 8 (NA‐1) lack the first 45 bp of the signal sequence, but considering the flow cytometry data the signal sequence must be functional allowing the membrane expression of this receptor allele. The part of the cDNA sequence of all isolated clones coding the mature FcγRIII is identical to the wild‐type sequence. Therefore, we conclude that the decreased expression of FcγRIII on granulocytes of this SLE patient is due to the transport defect of one of the receptor alleles.
Isotype switching in anti‐immunoglobulin‐activated B lymphoblasts: differential requirements for interleukin 4 and other lymphokines to elicit membrane vs. secreted IgG1
Authors: Purkerson Jeffrey M. , Isakson Peter C. 
Published: March 2007

AbstractAnti‐immunoglobulin (Ig)‐activated B lymphoblasts, prepared by culturing high‐density B cells with anti‐Ig‐Sepharose for 48 h, can be induced to secrete IgM and IgG1 by a mixture of T cell‐derived lymphokines containing interleukin (IL) 4. In this study we have examined the conditions required for lymphokine‐mediated induction of IgG1 secretion and membrane (m)IgG1 expression in B lymphoblasts. Resting B cells exposed to IL 4 (10–100 U/ml) during anti‐Ig‐mediated blast transformation did not secrete IgG1 upon subsequent culture with lipopolysaccharide (LPS) regardless of whether IL 4 was present or absent during the secondary culture. In contrast, B lymphoblasts previously exposed to IL 4 did secrete IgG1 in response to T cell‐derived lymphokines [EL 4 supernatant depleted of IL 4; (D)EL 4 SN]. However, optimal IgG1 secretion was obtained when B lymphoblasts were simultaneously exposed to IL 4 and other lymphokines. Pre‐exposure to (D)EL 4 SN, which contains IL 5 and IL 2, failed to prepare anti‐Ig blasts to secrete IgG1 in response to LPS and IL 4. Inhibition of IL 5 and IL 2 activity in EL 4 SN suppressed IL 4‐mediated IgG1 secretion. Together, these data indicate that B lymphoblasts require IL 5 and IL 2 in addition to IL 4 to secrete IgG1, and that the IL 4 signal(s) must precede or accompany those provided by the other lymphokines. As a measure of the fraction of cells capable of switching to IgG1, we assessed expression of mIgG1 on B lymphoblasts by fluorescence flow cytometry. B lymphoblasts cultured for 3 days with (D)EL 4 SN and IL 4 (10–100 U/ml) were 8% to 20% mIgG1+; in the absence of IL 4 blasts did not express detectable mIgG1. Although anti‐Ig blasts treated with LPS and IL 4 did not secrete appreciable IgG1, a substantial fraction of B lymphoblasts (4%–19%) cultured with LPS and IL 4, but not LPS alone, expressed mIgG1. These results suggest that LPS and IL 4 are sufficient to commit B lymphoblasts to mIgG1 expression, but that additional signals provided by T cell‐derived lymphokines are required to elicit IgG1 secretion.
Isoforms of the E2 molecule: D44 monoclonal antibody defines an epitope on E2 and reacts differentially with T cell subsets
Authors: Gelin Catherine , Zoccola Didier , Valentin Hélène , Raynal Brigitte , Bernard Alain 
Published: March 2007

AbstractHuman T cell rosetting with erythrocytes is clearly dependent on the CD2‐CD58 interaction. We have previously demonstrated that other T cell molecules are involved in the rosette phenomenon, including the E2 molecule, a 32‐kDa transmembrane glycoprotein. In this report we show that the D44 monoclonal antibody (mAb), previously shown to subdivide T cells into subpopulations with distinct functional repertoires and to identify 70% of lymphocytes from bronchoalveolar lavage from HIV+ patients, defined a new epitope on the E2 molecule. This was illustrated by the reactivity of the D44 mAb in Western blot experiments performed with the immunoaffinity purified E2 molecule. Moreover, double‐labeling experiments showed that the E2 molecule exhibited varying epitopes when expressed in different cell types. The D44 and 12E7 epitopes were restricted to distinct subpopulations of T cells and, more importantly, the D44 expression was limited to the CD29+ population including the memory subset. The O662 and L129 epitopes are present on all T cells. Thus, the E2 molecule has both common and variable epitopes in its extracellular domain, and only the common epitopes seem to be involved in T cell adhesion processes.
A lectin‐binding soluble factor released by CD8+CD57+ lymphocytes from AIDS patients inhibits T cell cytotoxicity
Authors: Sadat‐Sowti Behazine , Debré Patrice , Guillon Jean‐Marcel , Hadida Fabienne , Autran Brigitte , Idziorek Thierry , Okzenhendler Eric , Katlama Christine , Mayaud Charles 
Published: March 2007

AbstractCD8+CD57+ T cells, expanded in peripheral blood lymphocytes of AIDS patients, inhibit the effector phase of HLA‐specific cytotoxic T lymphocytes, natural killer and lymphocyte‐activated killer cells in a 4‐h chromium‐release assay. This inhibitory activity present in supernatants of purified sorted CD8+CD57+ cells is mediated by a non‐antigen‐specific inhibitory factor which is distinct from prostaglandin E2, T cell growth factor (TGF)‐β, latent‐TGF‐β, tumor necrosis factor (TNF)‐α and TNF‐β. Partial biochemical characterization demonstrates that the CD8+CD57+ inhibitory activity (a) is heat, trypsin and acid resistant, (b) binds to concanavalin A columns, indicating its glycosylation state and (c) is mediated by a 20–30‐kDa soluble molecule.