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The Facility for Antiproton and Ion Research (FAIR) is in its ï¬nal construction stage next to the campus of the Gesellschaft für Schwerionenforschung Helmholtzzentrum for heavy-ion research in Darmstadt, Germany. Once it starts its operation, it will be the main nuclear physics research facility in many basic sciences and their applications in Europe for the coming decades. Owing to the ability of the new fragment separator, Super-FRagment Separator, to produce high-intensity radioactive ion beams in the energy range up to about 2 GeV/nucleon, these can be used in various nuclear reactions. This opens a unique opportunity for various nuclear structure studies across a range of ï¬elds and scales: from low-energy physics via the investigation of multi-neutron systems and halos to high-density nuclear matter and the equation of state, following heavy-ion collisions, fission and study of short-range correlations in nuclei and hypernuclei. The newly developed reactions with relativistic radioactive beams (R3B) set up at FAIR would be the most suitable and versatile for such studies. An overview of highlighted physics cases foreseen at R3B is given, along with possible future opportunities, at FAIR. This article is part of the theme issue 'The liminal position of Nuclear Physics: from hadrons to neutron stars'.
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Experimental studies of nuclear fission induced by fusion, transfer, spallation, fragmentation, and electromagnetic reactions in combination with state-of-the-art calculations are successful to investigate the nuclear dissipation mechanism in normal nuclear matter, containing only nucleons. The dissipation mechanism has been widely studied by the use of many different fission observables and nowadays the dissipation coefficients involved in transport theories are well constrained. However, the existence of hypernuclei and the possible presence of hyperons in neutron stars make it necessary to extend the investigation of the nuclear dissipation coefficient to the strangeness sector. In this Letter, we use fission reactions of hypernuclei to constrain for the first time the dissipation coefficient in hypernuclear matter, observing that this coefficient increases a factor of 6 in the presence of a single Λ hyperon with respect to normal nuclear matter.
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Taking benefit of the R3B/SOFIA setup to measure the mass and the nuclear charge of both fission fragments in coincidence with the total prompt-neutron multiplicity, the scission configurations are inferred along the thorium chain, from the asymmetric fission in the heavier isotopes to the symmetric fission in the neutron-deficient thorium. Against all expectations, the symmetric scission in the light thorium isotopes shows a compact configuration, which is in total contrast to what is known in the fission of the heavier thorium isotopes and heavier actinides. This new main symmetric scission mode is characterized by a significant drop in deformation energy of the fission fragments of about 19 MeV, compared to the well-known symmetric scission in the uranium-plutonium region.
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Spectroscopic factors of neutron-hole and proton-hole states in ^{131}Sn and ^{131}In, respectively, were measured using one-nucleon removal reactions from doubly magic ^{132}Sn at relativistic energies. For ^{131}In, a 2910(50)-keV γ ray was observed for the first time and tentatively assigned to a decay from a 5/2^{-} state at 3275(50) keV to the known 1/2^{-} level at 365 keV. The spectroscopic factors determined for this new excited state and three other single-hole states provide first evidence for a strong fragmentation of single-hole strength in ^{131}Sn and ^{131}In. The experimental results are compared to theoretical calculations based on the relativistic particle-vibration coupling model and to experimental information for single-hole states in the stable doubly magic nucleus ^{208}Pb.
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Fifty-five inclusive single nucleon-removal cross sections from medium mass neutron-rich nuclei impinging on a hydrogen target at â¼250 MeV/nucleon are measured at the RIKEN Radioactive Isotope Beam Factory. Systematically higher cross sections are found for proton removal from nuclei with an even number of protons as compared to odd-proton number projectiles for a given neutron separation energy. Neutron removal cross sections display no even-odd splitting, contrary to nuclear cascade model predictions. Both effects are understood through simple considerations of neutron separation energies and bound state level densities originating in pairing correlations in the daughter nuclei. These conclusions are supported by comparison with semimicroscopic model predictions, highlighting the enhanced role of low-lying level densities in nucleon-removal cross sections from loosely bound nuclei.
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Excitation spectra of ^{11}C are measured in the ^{12}C(p,d) reaction near the η^{'} emission threshold. A proton beam extracted from the synchrotron SIS-18 at GSI with an incident energy of 2.5 GeV impinges on a carbon target. The momenta of deuterons emitted at 0° are precisely measured with the fragment separator (FRS) operated as a spectrometer. In contrast to theoretical predictions on the possible existence of deeply bound η^{'}-mesic states in carbon nuclei, no distinct structures are observed associated with the formation of bound states. The spectra are analyzed to set stringent constraints on the formation cross section and on the hitherto barely known η^{'}-nucleus interaction.
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During the study of autoimmune models we found that (SWR x SJL)F1 mice (both parental strains with the V beta a phenotype) spontaneously produced immunoglobulin G (IgG) antibodies directed against Sm/U1 small nuclear ribonucleoproteins (snRNPs). In some of these females, the presence of these autoantibodies was found as early as 10 wk of age. Their frequency increased with age i.e., 70% at 40 wk. At that time, only 10% of males developed anti-Sm/U1snRNP antibodies. Anti-Sm/U1snRNP antibodies from positive mice generally recognized the peptides BB', D, 70 kD, and A from RNPs. These polypeptides are known to bear the autoantigenic epitopes that are recognized by human sera containing anti-Sm and anti-U1snRNP antibodies. Reactivity of IgG antibodies with the octapeptide sequence PPPGMRPP was also found in 30% of anti-Sm/U1snRNP positive (SWR x SJL)F1 mice that precipitated BB' peptides. This octapeptide has been described as the most immunoreactive linear epitope in systemic lupus erythematosus (SLE) patients with anti-Sm and anti-U1snRNP antibodies. Approximately 30% of anti-Sn/U1snRNP positive females, later produced anti-dsDNA antibodies. This fact was accompanied by the development of proteinuria due to glomerulonephritis mediated by immunocomplexes. In addition to the specific autoimmune response, (SWR x SJL)F1 females also showed other immunologic abnormalities such as hypergammaglobulinemia, and an approximately twofold increase in spleen cell number compared with control mice. These results indicate that (SWR x SJL)F1 females develop clinical and serological abnormalities similar to those observed in human SLE and constitute a novel model for the study of the genetic mechanisms that result in autoimmunity.
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Modelos Animais de Doenças , Lúpus Vulgar , Animais , Antígenos/imunologia , Biomarcadores , Feminino , Imunofluorescência , Células HeLa , Humanos , Imunoglobulina G/imunologia , Lúpus Vulgar/imunologia , Lúpus Vulgar/fisiopatologia , Masculino , Camundongos , Camundongos Endogâmicos , RNA Nuclear Pequeno/imunologiaRESUMO
The present study describes an adult male who has had recurrent episodes of pulmonary infiltrates with severe acute respiratory failure over a period of 10 yrs. Clinical and pathological characteristics revealed bronchiolitis obliterans with organising pneumonia (BOOP) that responded dramatically to prednisone. BOOP is characterised by inflammation of the bronchioles and surrounding tissue in the lungs. It can mimic infectious pneumonia but diagnosis is suspected when there is no response to multiple antibiotic treatment, and blood and sputum cultures are negative for microorganisms. A high proportion of double-positive (DP)-T-cells was detected in peripheral blood and in bronchoalveolar lavage, expressing CD4 and CD8alphabeta heterodimer with memory phenotype. These DP-T-lymphocytes expressed specific homing molecules that could explain their tropism to lung tissue, giving rise to the clinical symptoms. The patient did not present organomegaly, lymphadenopathy, lymphocytosis or other features of malignancy. However, T-cell receptor Vbeta chain analysis indicated clonal rearrangement, and cytogenetic studies displayed chromosomic alterations that were similar to clonal proliferation observed in ataxia-telangiectasia and T-prolymphocytic leukaemia. The findings suggest a smouldering form of lymphoproliferation, the first sign of which was bronchiolitis obliterans organising pneumonia requiring constant corticoid treatment.
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Pneumonia em Organização Criptogênica/complicações , Leucemia de Células T/complicações , Leucemia de Células T/diagnóstico , Adulto , Anti-Inflamatórios/uso terapêutico , Líquido da Lavagem Broncoalveolar/citologia , Linfócitos T CD4-Positivos , Linfócitos T CD8-Positivos , Pneumonia em Organização Criptogênica/sangue , Pneumonia em Organização Criptogênica/tratamento farmacológico , Humanos , Leucemia de Células T/classificação , Masculino , Prednisolona/uso terapêuticoRESUMO
CD8 glycoproteins play an important role in both the maturation and function of MHC class I-restricted T lymphocytes. A 25-year-old man, from a consanguineous family, with recurrent bacterial infections and total absence of CD8(+) cells, was studied. Ab deficiencies and ZAP-70 and TAP defects were ruled out. A missense mutation (gly90-->ser) in both alleles of the immunoglobulin domain of the CD8 alpha gene was shown to correlate with the absence of CD8 expression found in the patient and two sisters. Conversely, high percentages of CD4(-)CD8(-)TCR alpha beta(+) T cells were found in the three siblings. A novel autosomal recessive immunologic defect characterized by absence of CD8(+) cells is described. These findings may help to further understanding of the role of CD8 molecules in human immune response.
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Substituição de Aminoácidos , Antígenos CD8/genética , Síndromes de Imunodeficiência/genética , Mutação de Sentido Incorreto , Adulto , Animais , Formação de Anticorpos , Infecções Bacterianas/etiologia , Antígenos CD8/química , Células COS , Chlorocebus aethiops , Consanguinidade , Citotoxicidade Imunológica , Análise Mutacional de DNA , Dimerização , Feminino , Genes Recessivos , Genótipo , Humanos , Síndromes de Imunodeficiência/imunologia , Síndromes de Imunodeficiência/patologia , Masculino , Dados de Sequência Molecular , Mutação , Linhagem , Subunidades Proteicas , Proteínas Recombinantes de Fusão/imunologia , Recidiva , Roma (Grupo Étnico)/genética , Espanha , Subpopulações de Linfócitos T/imunologia , Subpopulações de Linfócitos T/patologia , TransfecçãoRESUMO
It has been previously described that some proteins containing HMG boxes are able to bind more strongly to DNA modified with cis-diamminedichloroplatinum (II) (cisplatin) than to unmodified DNA. In the present study, we analyzed the interaction of cisplatin-modified DNA with the human autoantigen NOR-90 (UBF), a transcription factor that contains several HMG boxes. Using autoantibodies against NOR-90 to perform ELISA and immunoprecipitation, it was confirmed that NOR-90 (UBF) was able to bind cisplatin-modified DNA more avidly than unmodified DNA or trans-diamminedichloroplatinum(II) (transplatin) modified DNA. Moreover, by Southwestern, we observed that the 97 kDalton isoform of NOR-90 (UBF1) was able to bind cisplatin-modified DNA more strongly than the 94 kDalton isoform (UBF2); binding of unmodified DNA or transplatin-modified DNA was not detected with either isoform. Sera containing autoantibodies against NOR-90 did not inhibit, but increased the binding of NOR-90 to cisplatin-modified DNA.
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Autoantígenos/metabolismo , Cisplatino/metabolismo , Adutos de DNA/metabolismo , Região Organizadora do Nucléolo/imunologia , Sítios de Ligação , Humanos , Proteínas Nucleares/metabolismoRESUMO
Mice injected at birth with semiallogeneic spleen cells develop a host-versus-graft disease (HVGD) characterized by the polyclonal activation of donor B cells by alloreactive host CD4+ T cells, the production of autoantibodies (autoAb) and the development of an inmmunocomplex-mediated glomerulonephritis. It has been demonstrated that the recognition of MHC class II, but not class I or non MHC, alloantigens triggers the development of the autoimmune syndrome (AIS). The finding of different expression patterns of Ia molecules in different mouse strains, and a closed restriction of some immune responses to particular H-2 haplotypes, prompted us to analyze whether variations in the expressed MHC class II molecules modify the HVGD. First, newborn BALB/c mice received spleen cells from F1 hybrid mice obtained by mating BALB/c mice with several mouse strains differing in the H-2 haplotype. Second, spleen cells from different F1 mice were neonatally injected in mice of both parental strains. All groups of BALB/c mice injected with different combinations of F1 mice showed an HVGD with a very similar serological course. However, in some instances, duration was different when comparing both parental strains injected with spleen cells from the mutual F1 hybrids. These results suggest that host MHC, but not donor MHC haplotype may modulate the AIS associated with the induction of neonatal tolerance.
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Antígenos H-2/imunologia , Reação Hospedeiro-Enxerto/imunologia , Tolerância Imunológica , Isoantígenos/imunologia , Animais , Animais Recém-Nascidos , Doenças Autoimunes , Haplótipos , Camundongos , Camundongos Endogâmicos , Baço/citologia , Baço/imunologiaRESUMO
Superantigens (SAg) are bacterial exotoxins that provoke extreme responses in the immune system; for example, the acute hyperactivation of SAg-reactive T cells that leads to toxic shock syndrome is followed within days by strong immunosuppression. The gamma interferon (IFN-gamma) response is deeply affected in both extremes. The implication of IFN-gamma in the pathophysiology of lethal shock induced in mice after a secondary challenge with the SAg staphylococcal enterotoxin B (SEB) prompted us to study the regulation of IFN-gamma secretion and the intracellular response. We demonstrate in this study that a rechallenge with SEB becomes lethal only when given inside a critical time window after SEB priming and is associated with an increase of IFN-gamma serum release 72 h after priming. However, at this time, a selective blockade of IFN-gamma/STAT1 signaling develops in spleen cells, correlating with a lack of expression of the IFN-gamma receptor beta subunit and STAT1 in the T-cell population. Selective blockade of the STAT1 signaling pathway--while simultaneously maintaining STAT3 signaling and expression--may be a protective mechanism that shortens IFN-gamma production during the Th1 effector response. This blockade may also have consequences on switching towards a suppressor phenotype with chronic exposure to the superantigen.
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Antígenos de Bactérias/imunologia , Enterotoxinas/imunologia , Receptores de Interferon/biossíntese , Fator de Transcrição STAT1/metabolismo , Transdução de Sinais/imunologia , Células Th1/imunologia , Animais , Ensaio de Desvio de Mobilidade Eletroforética , Escherichia coli/imunologia , Tolerância Imunológica , Interferon gama/biossíntese , Ligantes , Ativação Linfocitária/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fator de Transcrição STAT1/imunologia , Choque Séptico/imunologia , Superantígenos/imunologia , Receptor de Interferon gamaRESUMO
During the effector phase of graft-versus-host disease (GvHD) response, donor T cells play an essential role and they are believed to change the expression of activation and co-stimulatory markers associated with functional alloreactivity. We analysed the expression of CD25, CD69, HLA-DR, CD154 and CD134 on CD4+ and CD8+ T cells by flow cytometry during acute GvHD (aGvHD) in 24 patients receiving human leucocyte antigen (HLA)-identical stem cell transplants. Expression of these molecules in nine patients with stages I-IV aGvHD was compared with 15 patients without aGvHD (n = 15). Serial analysis showed that peripheral blood of aGvHD patients presented a significant increase of CD4+ CD25+ cells (P < 0.03), CD4+ CD69+ (P < 0.04) and CD4+ CD134+ cells (P < 0.01). Additionally, there was a significant increase in CD8+ cells expressing CD134 (P = 0.007) and CD154 (P = 0.02). After resolution of aGvHD, the increased expression of these molecules returned to values comparable to patients without aGvHD. Only two of the 15 patients without clinical signs of aGvHD presented activated T cells that could not be attributed to development of aGvHD. In summary, our data show that multiple activation molecules are preferentially up-regulated on CD4+ and CD8+ T cells from patients with aGvHD. These patients had a significant increase in the expression of the co-stimulatory molecules CD134 and CD154.
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Complexo CD3/imunologia , Doença Enxerto-Hospedeiro/imunologia , Linfócitos T/imunologia , Doença Aguda , Adulto , Antígenos CD/análise , Antígenos de Diferenciação de Linfócitos T/análise , Biomarcadores/sangue , Linfócitos T CD4-Positivos/imunologia , Ligante de CD40/análise , Linfócitos T CD8-Positivos/imunologia , Estudos de Casos e Controles , Feminino , Citometria de Fluxo , Antígenos HLA-DR/análise , Humanos , Lectinas Tipo C , Ativação Linfocitária/imunologia , Masculino , Pessoa de Meia-Idade , Receptores de Interleucina-2/análise , Receptores OX40 , Receptores do Fator de Necrose Tumoral/análise , Estatísticas não ParamétricasRESUMO
HnRNP antigen from HeLa cells was purified using a monoclonal antibody (383 IgM) that recognizes heterogeneous nuclear ribonucleoprotein (hnRNP). From extracts of HeLa cells radiolabelled with 32P, this antibody immunoprecipitates relatively large RNAs of heterogeneous size which are synthesized in the presence of actinomycin D at doses which suppress synthesis of ribosomal RNAs (characteristic features of heterogeneous nuclear RNA). In immunoblots, 383 IgM binds to seven polypeptides: one of approximately 23,000 daltons, three between 30,000 and 43,000 daltons which correspond to the known hnRNP polypeptides called A1, A2 and C1, one of approximately 50,000 daltons, and a doublet of approximately 120,000 daltons. These proteins comigrate through sucrose density gradients suggesting that they are physically associated. Thus, 383 IgM appears to define an epitope that is shared among a number of the protein components of hnRNP. This antibody has been used to design a simple and fast protocol which allows the determination of autoantibodies from human sera by ELISA.
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Antígenos/imunologia , Autoanticorpos/análise , Ribonucleoproteínas Nucleares Heterogêneas Grupo A-B , Ribonucleoproteínas Nucleares Heterogêneas Grupo C , RNA Nuclear Heterogêneo/imunologia , Ribonucleoproteínas/imunologia , Animais , Anticorpos Monoclonais/imunologia , Dactinomicina/farmacologia , Ensaio de Imunoadsorção Enzimática , Epitopos , Imunofluorescência , Células HeLa , Ribonucleoproteína Nuclear Heterogênea A1 , Ribonucleoproteínas Nucleares Heterogêneas , Humanos , Imunoglobulina M/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Peso MolecularRESUMO
We describe an autoantibody specificity present in a subgroup of patients with a severe form of autoimmune chronic active hepatitis. These antibodies precipitate a 90-nucleotide RNA from human whole cell extracts and recognize a 48-kDa polypeptide in immunoblotting assays. The RNA is a UGA suppressor serine tRNA that carries selenocysteine (tRNA[Ser]Sec)), as shown by sequence analysis. The protein does not appear to be seryl-tRNA synthetase; rather, it is an excellent candidate for a factor involved in cotranslational selenocysteine incorporation in human cells.
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Autoanticorpos/imunologia , Autoantígenos/química , Doenças Autoimunes/imunologia , Hepatite Crônica/imunologia , RNA de Transferência de Serina/metabolismo , Ribonucleoproteínas/imunologia , Selenocisteína/metabolismo , Sequência de Bases , Genes Supressores , Humanos , Dados de Sequência Molecular , Aminoacilação de RNA de TransferênciaRESUMO
We established chronic graft vs host disease in (BALB/c x A/J) F1 mice with the injection of lymphoid cells from the parental A/J strain. These animals developed glomerulonephritis, forefoot edema, alopecia, splenomegaly, and lymphadenopathy to various degrees, and all developed antinuclear antibodies. To determine whether these antibodies were directed against the small nuclear ribonucleoprotein (snRNP) particles that are characteristic targets for autoimmune responses in human rheumatic diseases, sera were studied in the 32P immunoprecipitation and immunoblotting assays. Among 20 mice, antibodies to snRNP developed in 10. These antibodies usually reached maximal levels about 4 wk after induction of graft vs host disease and generally fell thereafter. However, two mice developed antibodies to snRNP between the 10th and 20th wk of follow-up. Sera from six mice strongly recognized the U1 snRNP and an additional serum strongly bound both the U1 and U3 particles. Several sera contained lower levels of antibodies specific for the U3 and possibly pre-U2 snRNP particles. In immunoblots, sera that immunoprecipitated the U1 snRNP bound epitopes located on its 70,000 Da, A, B'/B, and/or C polypeptides. Sera that immunoprecipitated the U3 snRNP recognized a 34,000-Da polypeptide. These polypeptides are known to bear the autoantigenic epitopes that are recognized by human sera containing anti-U1 RNP and anti-U3 RNP autoantibodies. We conclude that chronic graft vs host disease in mice provides a model for the study of the autoimmune responses that characterize human diseases such as mixed connective tissue disease, scleroderma, and SLE.
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Autoanticorpos/biossíntese , Modelos Animais de Doenças , Doença Enxerto-Hospedeiro/imunologia , RNA Nuclear Pequeno/imunologia , Animais , Reações Antígeno-Anticorpo , Sítios de Ligação de Anticorpos , Cruzamentos Genéticos , Feminino , Doença Enxerto-Hospedeiro/genética , Imunoensaio , Camundongos , Camundongos Endogâmicos A , Testes de Precipitina , RNA Nuclear Pequeno/isolamento & purificaçãoRESUMO
We established chronic graft vs host disease (GVHD) in (C57BL/10 x DBA/2)F1 mice with an injection of lymphoid cells from the parental DBA/2 strain. In addition to Abs earlier reported, of the 20 animals studied 13 developed Abs against transfer RNA/protein particles. Ten of the 13 sera immunoprecipitated a similar-sized RNA that co-migrated in PAGE with isoleucine tRNA. In immunoblots against proteins affinity purified using anti-isoleucyl-tRNA synthetase prototype serum, 7 of the 10 sera reacted with a polypeptide of 76 kDa that was similar in size to a protein recognized by a human anti-isoleucyl-tRNA synthetase serum. Three of 10 sera significantly and specifically inhibited isoleucyl-tRNA synthetase enzyme activity and one inhibited lysyl-tRNA synthetase activity. These data suggest that the autoantibodies to tRNA-associated proteins that develop in GVHD mice may react with amino acyl-tRNA synthetases, particularly those belonging to the multienzyme complex. Such autoantibodies are associated with myositis in humans, and these mice showed evidence compatible with myositis that appeared to be a manifestation of their GVHD. No previous example of spontaneous development of antisynthetases in animals has been described. We also demonstrated the presence of Abs against the NOR:90 nucleolar Ag as a new target in chronic GVHD. We conclude that chronic GVHD in mice provides a model for the study of the autoimmune responses that characterize human diseases such as mixed connective tissue disease, scleroderma, SLE, and myositis with a wider autoantibody response than that described so far.
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Autoanticorpos/análise , Doença Enxerto-Hospedeiro/imunologia , RNA de Transferência/imunologia , Ribonucleoproteínas Nucleares Pequenas/imunologia , Animais , Nucléolo Celular/imunologia , Doença Crônica , Imunofluorescência , Immunoblotting , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Endogâmicos DBA , Testes de PrecipitinaRESUMO
We identified a patient (CAG) with scleroderma whose serum contained a high titer of IgG class antibodies that stained nucleoli in a pattern of independent tiny spots. When tested on isolated chromosomes, these antibodies selectively stained the nucleolus-organizing regions (NOR) of chromosomes 13, 14, 15, 21, and 22. These staining patterns were not altered when substrate cells and chromosomes were treated with RNase, 0.1 M HC1, or 4 M urea, but they were abolished by treatment with DNase and trypsin. Immunoblots performed with serum CAG on isolated nucleolar substrates identified a protein antigen of approximately 90 kDa. Antibodies affinity-purified from this protein selectively stained nucleoli and NOR chromosomal regions. Therefore, this protein is the antigen that accounts for the ability of serum CAG to recognize the NOR. In a search for the NOR 90-kDa specificity among 254 patients with various rheumatic diseases, we found nine additional patients whose sera stained metaphase chromosomes selectively at the NOR. Sera from five of them (three with scleroderma, two of unknown diagnosis) recognized a protein that electrophoretically co-migrated with the CAG antigen. Thus, scleroderma is present in at least four of six who appear to have this specificity. We conclude that autoantibodies to the NOR 90-kDa antigen have an association with scleroderma and may be useful diagnostically and as a probe for further studies of the biology of the cell nucleolus.
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Autoanticorpos/imunologia , Autoantígenos/imunologia , Cromatina/imunologia , Doenças do Tecido Conjuntivo/imunologia , Proteínas Nucleares/imunologia , Região Organizadora do Nucléolo/imunologia , Escleroderma Sistêmico/imunologia , Imunofluorescência , Peso MolecularRESUMO
We previously described autoantibodies against a UGA serine tRNA-protein complex (tRNP(Ser)Sec) in patients with type-1 autoimmune hepatitis [1] and now define the specificity and frequency of this autoantibody and the DNA sequence encoding the tRNA(Ser)Sec-associated antigenic protein. The presence of anti-tRNP(Ser)Sec antibodies was highly specific for type-1 autoimmune hepatitis, as 47.5% of patients were positive compared with none of the control subjects. To characterize the antigenic protein(s), we immunoscreened a human cDNA library with anti-tRNP(Ser)Sec-positive sera. Two clones (19 and 13) were isolated. Clone 19 encodes a protein with a predicted molecular mass of 48.8 kD. Clone 13 is a shorter cDNA, almost identical to clone 19, which encodes a 35.9-kD protein. Expression of both cDNAs was accomplished in Escherichia coli as His-tagged recombinant proteins. Antibodies eluted from both purified recombinant proteins were able to immunoprecipitate the tRNA(Ser)Sec from a HeLa S3 cell extract, demonstrating their cross-reactivity with the mammalian antigenic complex. Recent cloning data relating to the target antigen(s) of autoantibodies in autoimmune hepatitis patients that react with a soluble liver antigen (SLA) and a liver-pancreas antigen (LP) have revealed that these two autoantibodies are identical and that the cloned antigen shows 99% amino acid sequence homology with tRNP(Ser)Sec.