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AbstractJapanese activities on fusion structural materials R & D have been well organized under the coordination of university programs and JAERI/NIMS programs more than two decades. Where, two categories of structural materials have been studied, those are; reduced activation martensitic/ferritic steels (RAFs) as reference material and vanadium alloys and SiC/SiC composite materials as advanced materials. The R & D histories of these candidate materials and the present status in Japan are reviewed with the emphasis on materials behavior under radiation damage. The on-going Japan-USA collaborations on blanket engineering and materials, JUPITER-II Program and on neutron radiation effects, JAERI/ORNL Phase IV and V are also presented.

Abstract Microstrucutral development and swelling behaviour of F82H (Fe-8Cr-2W-0.2V-0.04Ta-0.1C) steels irradiated at 435°C by dual beams of 10.5 MeV Fe³⁺ and 1.05 MeV He⁺ ions to 50 displacement per atoms (dpa) were investigated. The specimens used were F82H-std steel tempered at 750°C for 60 min and 40% cold-worked F82H-std (F82H + CW). The irradiation of helium atoms was controlled to implant in depths from 0.5 to 1.3 µm using an energy degrader with aluminium foil. The ratio of helium concentration to dpa was about 10 appmHe dpa^-1. Many small bubbles of 2-9 nm in F82H-std and 2-6 nm in F82H + CW were observed between about 0.1 and 1.8 µm from the surface. Swelling in F82H-std and F82H + CW was 0.1 and 0.06%, respectively, and was suppressed in cold-worked materials. Some micro-polycrystallines in the F82H-std were formed in only the irradiated range by the irradiation, and many were formed in F82H + CW steel. The sizes of the micro-polycrystallines in F82H-std and F82H + CW steels were about 0.5 and 0.3 µm, respectively.

ABSTRACTWe investigated tritium (T) release behavior from silica glass. The specimens were 8 kinds of commercially available silica glass. T was injected by the 6Li (n,α)T reaction of sintered pellets of lithium oxide (Li2O) into the silica glass with thermal neutrons in JRR-2 (VT-8) up to 5 × 1018neutrons/cm2at ambient temperature (about 350 K). After irradiation, the Li2O pellets were removed from the silica glass, and T release from the silica glass was measured in a flow of hydrogen (H2) or ammonia (NH3) sweep gas at atmospheric pressure at a constant heating rate of 2 K/min between 675 K and 1375 K with a proportional counter. In the case of H2sweep gas, a maximum tritium release rate was observed around 1023 K, while in the case of NH3sweep gas, two peaks around 1023 K and around 1123 K or a peak around 1123 K with a shoulder were obserbed. After the experiments of T release, FT-IR spectra showed a decrease of SiOH bands at 3650 cm−1. On the other hand, no changes in intensities at 2250 cm−1due to SiH were observed for both samples before and after T release.

The inherent properties of reduced activation ferritic/martensitic (RAFM) steels include reduced swelling and high recycling potential, which make them likely candidates for application in commercial fusion power plants. The International Energy Agency (IEA) agreement has been an effective framework for international co-operation in developing RAFM steels. The progress and critical issues observed in this co-operation are reported. The production of RAFM steels on an industrial scale has been demonstrated. Various methods of fusion welding and solid hot isostatic pressing (HIP) are feasible for joining the steels. Manufacturing of complex shapes with the powder HIP method works well for RAFM steels. Major critical issues addressed concern the effects of simultaneous introduction of helium and displacement damage. The availability of a 14 MeV neutron source is identified as an essential tool to determine this effect. Finally, the potential of oxide dispersion strengthening to increase the operating temperature of RAFM steels is considered as an issue that has to be resolved to enlarge the application temperature window of RAFM steels.

Plastically deformed microstructures in neutron-irradiated austenitic stainless steel were investigated by transmission electron microscopy (TEM). Neutron irradiation at 60°C and 330°C to about 7 dpa induced a high number density of faulted loops and black dots, which resulted in irradiation-induced hardening. In the specimen irradiated at 60°C and tensile tested at 25°C at a strain rate of 4×10−4s−1, the deformation microstructure consisted of twins, elongated faulted loops, and lath and twin martensite phase. In the specimens irradiated and tested at 330°C at a strain rate of 4×10−4and 4×10−6s−1, in addition to these features, dislocation channeling was also observed. The TEM examination suggests that lath and twin martensite can form during tensile testing at both of these temperatures. Examination of the specimens irradiated and tensile tested at 330°C indicated that twinning was the predominant deformation mode at slower strain rate and dislocation channeling was favored at higher temperature. From the micrographs taken from the {111} plane streak in a diffraction pattern, it is suggested that faulted loops could be the principal twin initiation site during deformation.

The importance of interactions between fusion materials research and development (R&D) and other technologies is emphasized to make attractive and realistic fusion technology integration activities. The focuses are on: (1) materials design and processing, (2) safety issues relating to materials and (3) material performance evaluation methodologies, including 14 MeV neutron source utilization for fusion material R&D. As typical examples, material design activities on reduced activation ferritic steels, vanadium alloys and SiC/SiC composite materials are provided. The safety assessment of reactor systems and reactor design code consideration including prediction methodologies of materials performance are also discussed.

The lymphocyte activation gene 3 (LAG-3), expressed in human activated T and natural killer (NK) cells, is closely related to CD4 at the gene and protein levels. We report here the initial characterization of the LAG-3-encoded protein. We have generated two monoclonal antibodies after immunization of mice with a 30-amino acid peptide that corresponds to an exposed extra loop region present in the LAG-3 immunoglobulin-like first domain. The reactivity of these reagents is directed against LAG-3 since they recognize both membrane-expressed and soluble recombinant LAG-3 molecules produced in a baculovirus expression system. The two antibodies are likely to react with the same or closely related epitope (termed LAG-3.1) exposed on the LAG-3 first domain extra loop, as assessed in competition experiments on LAG-3-expressing activated lymphocytes. Cellular distribution analysis indicated that the LAG-3.1 epitope is expressed on activated T (both CD4+ and CD8+ subsets) and NK cells, and not on activated B cells or monocytes. In immunoprecipitation experiments performed on activated T and NK cell lysates, a 70-kD protein was detected after SDS-PAGE analysis. 45-kD protein species were also immunoprecipitated. Both the 70- and 45-kD proteins were shown to be N-glycosylated. In Western blot analysis, only the former molecule was recognized by the anti-LAG-3 antibodies, demonstrating that it is LAG-3 encoded. These anti-LAG-3 antibodies were used to investigate whether the LAG-3 protein interacts with the CD4 ligands. By using a high-level expression cellular system based on COS-7 cell transfection with recombinant CDM8 vectors and a quantitative cellular adhesion assay, we demonstrate that rosette formation between LAG-3-transfected COS-7 cells and human leukocyte antigen (HLA) class II-bearing B lymphocytes is specifically dependent on LAG-3/HLA class II interaction. In contrast to CD4, LAG-3 does not bind the human immunodeficiency virus gp120. This initial characterization will guide further studies on the functions of this molecule, which may play an important role in immune responses mediated by T and NK lymphocytes.

In the present study, we have characterized the reactivity of two mAbs that are directed at the human TCR-gamma/delta. These reagents, designated anti-A13 and anti-TiV delta 2, were found to recognize antigenic determinants encoded by the TCR V delta 1 and V delta 2 gene segments, respectively. Immunofluorescence analyses performed with the antibodies confirmed that, in the TCR-gamma/delta+ cell subpopulation, the expression of V delta 2+ delta chains is largely predominant, as compared with the V delta 1+ counterparts. However, these experiments led to an apparently discrepant finding. Indeed, the total number of cells recognized by the anti-A13 plus the anti-TiV delta 2 antibodies was often greater than that detected with anti-TCR-delta 1, a reagent specific for a constant epitope of the human delta chain. Further investigation showed that the presence of a sizeable peripheral lymphocyte subset coexpressing the BMA031 and the A13 epitopes. Because the former antibody is known to recognize an invariant antigenic determinant of the TCR-alpha/beta dimer, these results suggested that the V delta 1 gene segment may be expressed with either C delta or C alpha. This hypothesis was confirmed using T2, an IL-2-dependent BMA031+ A13+ polyclonal cell line developed from peripheral blood of a healthy adult donor. Indeed, T2 cells were found to have productively rearranged the V delta 1 gene. Together, results of Northern blot analysis and cDNA cloning indicated that V delta 1 was expressed in these cells as part of a 1.6-kb full-length message including J alpha-C alpha segments.

We have recently described an mAb, anti-Ti gamma A, that recognizes an antigenic determinant carried by a TCR gamma chain. This antibody binds to approximately 3% of human PBLs and delineates a CD2+, CD3+, TCR-alpha/beta-, CD4-, CD8+/-, CD5+, NKH1-, and HLA class II- subset. The present study was designed to identify the gene encoding the Ti gamma A epitope. A first analysis was carried out on a previously characterized TCR gamma + fetal-cloned cell line termed F6C7. It was found that F6C7 cells have one gamma rearrangement on each chromosome: one joins V gamma 3 to J gamma 1, and the second joins V gamma 9 to J gamma P. Because only the latter allele appeared to be transcribed in the F6C7 lymphocytes, these data strongly suggested that anti-Ti gamma A mAb is specific for either a V gamma 9 or a V gamma 9-J gamma P-encoded peptide. To confirm this point, we studied an additional series of 13 randomly selected Ti gamma A+ cloned cells derived from peripheral blood of three distinct adult individuals. Each one of these lymphocytes was shown to both possess and transcribe a V gamma 9-J gamma P-C gamma 1-rearranged gene. It is therefore concluded that a predominant subpopulation of CD3+ TCR-alpha/beta- human circulating T lymphocytes (namely, the subset defined by anti-Ti gamma A mAb) surface expresses a gamma protein with a limited potential of variability from one cell to another.

We have previously characterized a CD3+ T cell receptor (TCR) alpha/beta- human fetal cloned cell line, termed F6C7, which surface-expresses a CD3-associated gamma chain identified by anti-NKFi, an mAb with a restricted clonotypic reactivity. Here, we have produced an additional antibody, anti-Ti-gamma A, which recognizes a public epitope of the gamma molecule defined by anti-NKFi. Ti-gamma A is present on approximately 3% of circulating lymphocytes with a wide range (1-15%) among 30 healthy individuals tested. Two-color immunofluorescence experiments performed with anti-Ti-gamma A and BMA 031 mAb (a reagent specific for the TCR-alpha/beta receptor) showed that surface expression of Ti-alpha/beta and Ti-gamma A is mutually exclusive. Moreover, it was found that most Ti-gamma A+ cells are CD2+, CD3+, CD4-, CD5+, NKH1-, HLA class II-negative. In contrast, the expression of the CD8 molecule on these T lymphocytes appears to be variable from one individual to another. Finally, we found that Ti-gamma A+ cells represent a majority of peripheral lymphocytes that express CD3 proteins but not the TCR-alpha/beta heterodimer. The delineation of this unique lymphocyte subset should help further studies on the biology of cells with a CD3-associated gamma complex.

We have recently generated a series of gamma/delta T cell clones able to kill, after in vitro immunization, an Epstein-Barr Virus-transformed B cell line (designated E418) in a non-major histocompatibility complex-requiring fashion. A monoclonal antibody, termed anti-10H3, produced against E418 was selected by its ability to block these cytotoxic interactions. Further analysis indicated that the inhibitory effects of anti-10H3 were highly selective (i.e., no blocking activity with multiple control clones used as effector cells; no alteration of the natural killer-like function mediated by the relevant gamma/delta clones against 10H3+ tumor cells such as Rex). The molecule immunoprecipitated by anti-10H3, termed TCT.1, was characterized as a 43-kD protein broadly distributed in the hematopoietic system. The TCT.1 molecule has been further studied here by protein microsequencing. Results show that the TCT.1-derived peptide sequences are virtually identical to corresponding regions of Blast-1, a previously described surface protein with unknown function. The likely identity of the two molecules has been strengthened by analyzing the susceptibility of TCT.1 to phosphatidylinositol-specific phospholipase C digestion in light of the known anchorage of Blast-1 to the cell membrane through a glycosyl-phosphatidylinositol-containing lipid. The TCT.1/Blast-1-encoding gene is well characterized; it belongs to the immunoglobulin gene superfamily and it is located in the same band of chromosome 1 as the CD1 gene cluster. Together, these data further support the view that proteins distinct from the conventional class I/II histocompatibility molecules are involved in specific T cell recognition.

We have recently derived from human fetal blood (25 wks) a series of cloned cell lines that were selected for their ability to kill the conventional natural killer (NK) target cell K5621. It was found that a fraction of these clones express CD3 proteins but not the monomorphic Ti αβ determinant recognized by WT31 antibody1. One interleukin-2-dependent CD3+WT31−clone, termed F6C7, was used for immunization of mice to generate monoclonal antibodies directed at a potentially novel recognition receptor. It was shown that F6C7 cells, which transcribe Ti β but not Ti α genes, surface-express a clonotypic structure, termed NKFi2. Immunoprecipitations performed with anti-NKFi monoclonal antibody (mAb) indicated that the corresponding molecule is resolved in SDS-polyacrylamide gel electrophoresis (PAGE) as a single band of relative molecular mass ∼85,000 (Mr∼85K). After reduction, a major band was detected at 44K and a faint band was present at 41K2. The present study was designed to characterize this structure. It was found that NKFi represents either two 44K disulphide-linked γ (TCR) chains, or possibly one γ chain associated to an additional undetected molecule, and that the 4IK material corresponds to a partially glycosylated fraction of the γ protein. Anti-NKFi mAb both induces a specific autocrine pro-liferative response and blocks cytotoxic function, demonstrating that γ chains serve as functional receptor structures on subpopulations of normal human lymphocytes.

A low impurity Fe18Cr12Ni (HP) and its heats doped with Si and C (HP + Si and HP + C) were irradiated to 6.7 × 1024n/m2(E≫ 1 MeV) at 513 K. The slow strain rate tensile (SSRT) tests were carried out at a constant strain rate of 1.7 × 10−7s−1in high purity, 573 K water. Scanning electron microscopy on the fracture surface revealed that HP and HP + Si failed mainly by the intergranular stress corrosion cracking (SCC), while the major failure mode in HP + C was the transgranular SCC. All alloys exhibited radiation hardening. HP + Si exhibiting the smallest hardening showed uniform elongation of 17%, while HP and HP + C did not. Transmission electron microscopy was also carried out. Frank loops and unidentified small clusters were formed in HP and HP + C, while only small clusters were observed in HP + Si.

A series of six austenitic stainless steels and two ferritic alloys were irradiated sequentially in two research reactors where the neutron spectrum was tailored as a function of time to produce a He production rate typical of a fusion device. Irradiation began in the Oak Ridge Research Reactor where an atomic displacement level of 7.4 dpa was achieved and was then transferred to the High Flux Isotope Reactor for the remainder of the irradiation to a total displacement level of 19 dpa. Temperatures of 60 and 330°C are reported on. At 330°C irradiation creep was found to be linear in stress and fluence with rates in the range of 1.7–5.5 × 10−4% MPa−1dpa−1. Annealed and cold-worked materials exhibited similar creep rates. There is some indication that austenitic alloys with TiC or TiO precipitates had a slightly higher irradiation creep rate than those without. The ferritic alloys HT-9 and Fe-16Cr had irradiation creep rates about 0.5 × 10−4% MPa−1dpa−1. No meaningful data could be obtained from the tubes irradiated at 60°C because of damage to the tubes.

We have identified a novel human gene of the Ig superfamily, designated LAG-3. Expression of this gene is undetectable in resting PBL, while it is found (a 2-kb message) in activated T and NK cells. The LAG-3 gene includes eight exons; the corresponding cDNA encodes a 498-amino acid membrane protein with four extracellular IgSF domains. The first one belongs to the V-SET; it is particular since it includes an extra loop in the middle of the domain and an unusual intrachain disulphide bridge. The three other domains belong to the C2-SET. Strong internal homologies are found in the LAG-3 molecule between domains 1 and 3, as well as between domains 2 and 4. It is therefore likely that LAG-3 has evolved by duplication of a pre-existing gene encoding a two IgSF-domain structure. The compared analysis of LAG-3 and CD4, with respect to both their peptidic sequence as well as their exon/intron organization, indicated that the two molecules are closely related. This point is strengthened by the finding that both genes are located on the distal part of the short arm of chromosome 12.