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Biomedical subjects

K Tomonari

Publications and source records attributed to K Tomonari.

At least 55 records · Page 3Linked to original sources
PubMed1990

Correlation between the V beta 4+ CD8+ T-cell population and the H-2d haplotype.

The V beta 4+ T-cell population was examined with a newly established antibody, KT4, specific for V beta 4. Between 4.8% and 19.4% of CD3+ peripheral T cells from various inbred strains of mice or F1 hybrids expressed V beta 4. The CD4 T-cell population had higher numbers of V beta 4+ T cells (5.5%-20.6%) than the CD8 T-cell population (2.5%-10.7%). Deletion of certain V beta-expressing T cells due to the presence of the Mlsa antigen and/or the absence of certain Tcrb-V genes increased relative numbers of V beta 4+ T cells. The data suggest that V beta 4+ CD8+ T cells might be positively selected by H-2d molecules.

Animals↗
PubMed1990

Epitope-specific binding of CD8 regulates activation of T cells and induction of cytotoxicity.

Functions of the CD8 molecule were examined to determine whether CD8 is merely a ligand-binding molecule and/or is involved in signal transduction. Using KT112 (anti-CD8 beta), CD8 was demonstrated to transduce an activation signal leading to cytotoxicity. Conformational changes of the CD8 molecule might be responsible for the activation, because (i) KT15 (anti-monomorphic CD8 alpha), but not antibodies specific for polymorphic CD8 alpha determinants, abrogated KT112 (anti-CD8 beta)-induced cytotoxicity without blocking the binding of KT112, whilst (ii) KT112 (anti-CD8 beta) inhibited KT15 (anti-monomorphic CD8 alpha)-mediated augmentation of proliferation triggered by a V beta 11-specific antibody without blocking the binding of KT15.

Animals↗
PubMed1989

Two monoclonal antibodies specific for the T cell receptor V alpha 8.

Two monoclonal antibodies, KT50 and KT65, specific for V alpha 8 have been established. This was determined as follows: (a) 4 T cell clones, C6, R1, G22 and I9, out of 43 T cell clones with various antigen specificities, major histocompatibility complex restrictions and V beta usages not only bound KT50 and KT65 but also expressed V alpha 8 mRNA, (b) KT50 and KT65 precipitated molecules from the clone C6 similar to the T cell receptor molecules precipitated in C6 cells by KT11 (anti-V beta 11) or KTL2 (anti-Ti) and (c) KT50 and KT65 were mitogenic and induced cytotoxicity. All strains of mice so far examined have populations of KT50+ and KT65+ T cells of 1.4%-3.6% and 0.9%-2.6%, respectively. Different H-2 haplotypes were not observed to affect the number of cells expressing KT50 or KT65. In addition KT15 (anti-CD8), without cross-linking to KT50 or KT65, augmented proliferation triggered by KT50 or KT65.

Animals↗
PubMed1989

Minor transplantation antigens: their role in shaping the T cell repertoire.

Minor transplantation, or histocompatibility (H), antigens are the targets of host-versus-graft (hvg) and graft-versus-host (gvh) reactions that occur when organs or tissues are exchanged between members of the same species who, although genetically not identical, are matched for their major histocompatibility complex (MHC) encoded transplantation antigens. Genes encoding minor H antigens map outside the MHC, on a number of different chromosomes. Whilst gvh and hvg reactions against individual minor H antigens are relatively weak, certainly in comparison with such reactions against MHC antigens, the presence of multiple minor H differences (the situation encountered in man) gives rise to very vigorous reactions that can endanger the survival of graft or host, or both. This is the pathological role of minor H antigens and, indeed, it was this role which was first designated to the MHC antigens, before their physiological role as guidance molecules for T lymphocytes was discovered. Recently, a potential physiological role for minor H antigens has been uncovered by the finding that the presence of certain minor H alleles in mice leads to removal in the thymus (negative selection) of all those T cells expressing a particular T cell receptor (TCR) gene. Such cells therefore never reach the periphery, where they might otherwise give rise to autoimmune reactions. The T cell repertoire is thus moulded by at least some minor H antigens, which may therefore be regarded as non-MHC immune response genes. Furthermore, T cell receptor usage by T cells specific for allogeneic minor H antigens appears not to be representative of T cell receptor usage in the peripheral pool.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Mapping minor H genes.

The manner in which minor histocompatibility (H) antigens have been defined in mouse and man, in vivo and in vitro, is considered. Chromosomal mapping of minor H genes using T-cell clones is illustrated, with particular reference to the H-Y antigen gene, using the sex-reversing translocation Sxr of mouse and the Sxr' mutation derived from it. A number of minor H antigen-specific T-cell clones restricted by class I or class II major histocompatibility complex (MHC) molecules are described, together with information about their phenotypes and T-cell receptor usage.

Animals↗
PubMed1988

Down-regulation of the T cell receptor by a mitogenic anti-Thy-1 antibody.

Antigen-specific unresponsiveness lasting at least 2 weeks can be induced in a T cell clone by 24-h pretreatment with mitogenic anti-T cell receptor antibodies. In this report the relationship is explored between the antigen-specific unresponsiveness and activation pathways triggered via the T cell receptor and Thy-1: the latter pathway is dependent on the former. A mitogenic anti-Thy-1 antibody (KT16) made the T cell clone unresponsive to specific antigen and to an anti-T cell receptor antibody coupled to Sepharose. The unresponsiveness lasted for at least 7 days. However, cells made unresponsive to specific antigen in these ways (the T cell receptor and Thy-1) could be activated by both interleukin 2 and KT16. KT16 down-modulated the T cell receptor immediately after the pretreatment, but not on day 7 after the pretreatment. These facts indicate that the state of the unresponsiveness was caused by blocking transduction of an activation signal triggered by the T cell receptor to an activation pathway shared by the T cell receptor and Thy-1.

Animals↗
PubMed1988

T-cell receptor-specific monoclonal antibodies against a V beta 11-positive mouse T-cell clone.

Two monoclonal antibodies specific for the mouse T-cell receptor (Tcr) have been established by immunization with a V beta 11+ T-cell clone, clone C6. One is a rat antibody, KT11 (IgG2b, k), specific for the V beta chain of C6, V beta 11. This was demonstrated by the fact that the strain distribution pattern of KT11+ cells was similar to that of V beta 5, 8, 9, 11, 12, and 13 and that the gene that encodes the molecule detected by KT11 was closely linked to V beta 8 in (B10 X SJL)F1 X SJL backcross mice. Furthermore, V beta of C6 has been cloned from a lambda gt10 cDNA library and was demonstrated to be identical to the V beta 11 published sequences. All strains of mice that do not express major histocompatibility complex class II E molecules had higher numbers of KT11+ cells than E+ strains. The KT11+ population in A strain mice and its H-2 congenic strains, however, was not affected by the presence or absence of E molecules. The other is a mouse antibody, KTL2 (IgM), specific for the idiotope of the Tcr expressed on the clone C6. Both antibodies were mitogenic and induced cytotoxicity. Expression of epitopes detected by KT11 or KTL2 was down-modulated by a T3 epsilon-specific antibody 145-2C11.

Animals↗
PubMed1988

[The pathogenesis of adenocarcinoma of the stomach after successful radiotherapy of squamous cell carcinoma of the lower intrathoracic esophagus--case report].

A case of a gastric cancer developed 3 years and 11 months after radiotherapy for esophageal cancer is reported. A 76-year-old man with a squamous cell carcinoma of the lower intrathoracic esophagus had received 50 Gy of irradiation as treatment. Thereafter, signs of the esophageal cancer disappeared radiologically and endoscopically, and a pathological biopsy of specimens taken from the site revealed no further cancer cells. The patient remained well for 3 years and 11 months after radiotherapy, at which time he again was admitted to hospital, having been diagnosed as having a gastric cancer. On admission, an upper G-I series showed a shadow defect along the lesser curvature of the upper-middle stomach but no evidence of any stenosis in the lower intrathoracic esophagus. Endoscopically, the mucosal surface of the esophagus was normal, and biopsy specimens taken from the site in the esophagus that had been treated with irradiation 3 years 11 months ago revealed no recurrence of his esophageal cancer. Endoscopical examination of the stomach showed an infiltrative tumor with ulceration, and a subsequent histological examination revealed a poorly differentiated adenocarcinoma. Upon a laparotomy, a metastasis was detected in the perigastric and paraaortic lymph nodes and the cancer had invaded the retroperitoneum. The stomach could not be removed and he died 3 months after the laparotomy.

Adenocarcinoma↗
PubMed1987

Occurrence of peptic ulcer in the gastric tube used for esophageal replacement in adults.

Reported in this paper are two cases of peptic ulcer which developed in the gastric tube used for esophageal replacement following esophagectomy for esophageal tumors in adults. The results of our cases suggest that acid secretion from the mucosa of the gastric tube, in spite of truncal vagotomy and the state of the tube, seems to play important roles in the pathogenesis of peptic ulcer of the gastric tube after esophageal replacement, even though circulatory disturbances, due to postoperative irradiation and gastric tube formation, have been suspected as the cause. Therefore, in those cases of gastric tube stasis, surgical drainage of the gastric tube should be performed.

Adult↗
PubMed1986

Carcinoma in adenoma of the papilla of Vater.

Carcinoma in adenoma of the papilla of Vater is extremely rare. We now report a case of adenocarcinoma in adenoma of the papilla of Vater and the clinicopathological findings are discussed. A 73-year-old Japanese woman was endoscopically diagnosed as a case of carcinoma combined with adenoma of the papilla of Vater. She underwent pancreatoduodenectomy and the postoperative course was satisfactory. Histological examination of the resected tissues revealed a superficial adenocarcinoma in the adenoma of the papilla of Vater. In certain cases, carcinoma of the papilla of Vater may develop from a pre-existing adenoma in the region. Therefore, we recommend that pancreatoduodenectomy should be done when an adenoma presents in this region.

Adenocarcinoma↗
PubMed1986

T-cell and antibody typing of a mouse population segregating for Sxr and H-2 haplotype.

During investigation of the frequency of recombination of the testis determining gene, Tdy, and the minor histocompatibility antigen gene Hya on the Sxr segment in an outbred mouse stock, we identified two fertile males, one XY and the other XYSxr, which typed H-2k positive using the H-2b anti-H-2k monoclonal antibody HB50, but whose cells failed either to stimulate H-Y specific H-2k restricted T-cell clones, or to be killed by anti-H-2k or anti-H-2k restricted H-Y specific cytotoxic T cells. We investigated these two mice and their existing relatives, using H-2 and H-Y typing methods. The progeny of their test matings with H-2b homozygous C57BL/6 females were also investigated. The results indicate that the transmission of the Hya gene on the Y chromosomes from both mice, and the additional Hya gene on the Sxr segment of the carrier male, allowed for the expression of the H-Y antigen and its detection in the presence of an H-2 haplotype for which we had H-2 restricted H-Y specific typing cells (H-2b and H-2k). Furthermore, we identified the haplotype of the two original males as expressed in the H-2 homozygous and heterozygous F2 progeny as H-2q and discovered an unexpected cross reactivity of the monoclonal anti KkDk antibody HB13 with half the cells of H-2q homozygotes, but not qb heterozygotes.

Animals↗
PubMed1986

H-Y status of X/X Sxr' male mice: in vivo tests.

Sex reversed X/X male mice carrying Sxr or the variant Sxr' were typed for expression of the male specific histocompatibility antigen H-Y, by skin grafting and by in vitro cytotoxic and proliferative tests. The X/XSxr males, like X/Y males, were H-Y positive by in vitro testing, and failed to reject semi-syngeneic male skin grafts. In contrast X/XSxr' males, like X/X females, were H-Y negative and rejected semi-syngeneic, male skin. Spleen cells from X/Y males sensitized C57BL/10 female recipients to reject syngeneic male skin rapidly, whilst immunization with X/X female or X/XSxr' male cells failed to stimulate such second-set responses. These data suggest that the H-Y antigen detected by cytotoxic T cells is the same as that detected by graft rejection responses, that the Sxr' variant is not a tissue-specific regulatory mutation, and that X/XSxr' individuals do not express H-Y antigen but nevertheless develop as phenotypic males.

Animals↗
PubMed1986

[Choriocarcinoma of the stomach].

A 55-year-old Japanese man was admitted to our hospital in January 1985 complaining of epigastralgia. Radiologic and endoscopic examinations showed gastric carcinoma, but biopsy specimens taken by surgery showed the histologic pattern of choriocarcinoma. On autopsy, multiple metastatic sites wer observed, and histological examination of the primary and metastatic sites revealed choriocarcinoma. Primary gastric choriocarcinoma may develop from gastric cancer by retrodifferentiation.

Biopsy↗