Group B streptococcal endocarditis in infancy with a giant vegetation on the pulmonary valve.
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Echocardiography↗
Biomedical subjects
M Tsuchida
Publications and source records attributed to M Tsuchida.
Analysis of cell surface antigens on glucocorticoid-treated rat thymocytes with monoclonal antibodies.
The effects of glucocorticoid (GC) on thymocytes have been utilized to investigate the maturation and differentiation of thymocytes, but these experiments have mainly been performed on mouse thymocytes. We investigated the cell surface antigens expressed by LEW rat thymocytes during thymic reconstitution after GC treatment. Three-color flow cytofluorometric analysis of CD4, CD8 and the T cell antigen receptor (TCR alpha beta) clearly demonstrated that normal rat thymocytes contain CD4-8+ TCR alpha beta- and CD4+8- TCR alpha beta- cells. After GC treatment, we observed significant increases in the percentages of CD4-8+ TCR alpha beta- and CD4+8- TCR alpha beta- cells. The extent of the increase in the percentage of CD4-8+ TCR alpha beta- cells was greater than that of CD4+8- TCR alpha beta- thymocytes. Two-color analysis of TCR alpha beta and major histocompatibility complex (MHC) class I antigen showed that GC treatment significantly increased the percentage of TCR alpha beta- MHC class Ihi cells. Three-color analysis of CD4, CD8 and MHC class I demonstrated that normal rat thymocytes contain CD4-8- MHC class Ihi cells, which increased in number after GC treatment. These results indicate that rat thymocytes contain no fewer CD4-8+ TCR alpha beta- and CD4+8- TCR alpha beta+ cells than do mouse thymocytes, and that CD4-8+ TCR alpha beta- cells predominate over CD4+8- TCR alpha beta- cells in LEW rat thymus. Rat CD4-8- cells seemed to be divided into two subsets of TCR alpha beta- MHC class Ihi and TCR alpha beta- MHC class I- cells.
Animals↗
Induction of specific unresponsiveness to cardiac allografts by short-term administration of anti-T cell receptor alpha beta antibody.
Organ graft rejection is a T cell-dependent process in which activation of alloreactive T cells via the T cell receptor/CD3 complex is a critical step. Although treatment with anti-CD3 has been shown to prevent and reverse allograft rejection, there is little information available regarding the effects of immunotherapy using anti-TCR alpha beta mAb for rejection. In the present study, short-term preoperative treatment of rats with a mAb against alpha beta TCR (R73) completely prevented the rejection of cardiac allografts. These rats accepted second cardiac allografts from the same donor strain, but not from a third-party strain, without additional treatment. In mixed lymphocyte cultures, T cells from rats that had received cardiac grafts did not respond to donor-strain heart cells, but did respond to donor-strain spleen cells and third-party heart cells. These findings suggest that specific unresponsiveness to cardiac tissue was induced in R73-treated rats. Such unresponsiveness was induced only when rats were pretreated with the mAb and subsequently received a transplant. It is likely that administration of a small dose of R73 induced transient immunomodulation of TCR molecules, resulting in unresponsiveness to a subsequent cardiac allograft. Immunotherapy with mAb against TCR alpha beta is very effective, without apparent side effects, and may provide a new method for preventing graft rejection.
Animals↗
Successful prevention and treatment of autoimmune encephalomyelitis by short-term administration of anti-T-cell receptor alpha beta antibody.
To identify an effective immunotherapy for T-cell-mediated autoimmune diseases, prevention and treatment of experimental autoimmune encephalomyelitis (EAE) induced in Lewis rats was attempted by administering a monoclonal antibody (mAb), R73, which is specific for rat T-cell receptor (TcR) alpha beta. Short-term administration of R73 at relatively low doses before immunization with encephalitogenic antigen, myelin basic protein (MBP), prevented the development of EAE. However, treatment with anti-CD4 and anti-Ia mAb in the same protocol was ineffective. Flow cytometric analysis demonstrated that short-term administration of R73 resulted in transient down-regulation of the TcR molecules, whereas the number of CD2-expressing T cells was well preserved. Furthermore, the response to MBP of T cells isolated from rats that were pretreated with R73 and then immunized with MBP was strongly suppressed. On the other hand, the T-cell response of R73-pretreated rats to a third-party antigen which was immunized at a later period was not inhibited. These findings suggest that in vivo administration of a low dose of R73 protects rats from EAE by inducing anergy of MBP-reactive encephalitogenic T cells. Furthermore, R73 treatment which started on day 10 of the immunization (shortly before the day of onset of clinical signs) completely suppressed the induction of EAE and that which started on day 11 (the day of onset) hastened recovery. Since the phenotypes of the TcR V beta chain of encephalitogenic T cells are not so limited as previously believed, immunotherapy with mAb against the TcR alpha beta framework may be one of the best methods for treatment of T-cell-mediated autoimmune diseases.
Amino Acid Sequence↗
Effects of irradiation, glucocorticoid and FK506 on cell-surface antigen expression by rat thymocytes: a three-colour flow cytofluorometric analysis.
The expression of T-cell antigen receptor (TCR) alpha beta was investigated in rat CD4- CD8- thymocytes during thymic reconstitution after the exposure of animals to irradiation or glucocorticoid. The effect of the immunosuppressant FK506 on the expression of TCR alpha beta in rat CD4- CD8- thymocytes was also examined. The percentage of CD4- CD8- thymocytes constituted 2.6% of total thymocytes and that of CD4- CD8- TCR alpha beta high cells constituted 12.6% of CD4- CD8- thymocytes in normal adult Lewis rats. The percentage of CD4- CD8- TCR alpha beta high cells increased during thymic reconstitution after irradiation, and maximally constituted 28.6% of CD4- CD8- thymocytes on day 7. Similar results were obtained during thymic reconstitution after glucocorticoid treatment. In contrast, continuous treatment with FK506 for 7 days markedly decreased not only the percentages of CD4+ CD8- TCR alpha beta high and CD4- CD8+ TCR alpha beta high thymocytes, but also that of CD4- CD8- TCR alpha beta high thymocytes. These results indicate that rat CD4- CD8- thymocytes contain a subpopulation of mature (TCR alpha beta high) cells. The possible implications of the existence of this subpopulation with regard to thymocyte differentiation and maturation are discussed.
Animals↗
The effects of FK506 and dexamethasone on rat thymocyte differentiation.
We investigated the effects of FK506 and glucocorticoids (GC) on rat thymocytes using flow cytofluorometry. Rats were treated with GC (0.1 mg/body, by single injection), with FK506 (1 mg/kg/day, for 7 days), or with FK506 and GC. GC alone significantly decreased the percentage of CD4+8+ thymocytes and increased the percentages of CD4-8-, CD4+8- and CD4-8+ thymocytes on day 7. FK decreased the percentage of CD4+8- and CD4-8+ thymocytes and increased the percentage of CD4+8+ thymocytes on days 5 to 14. FK and GC induced a significant decrease in the number of CD4+8+ thymocytes greater than that seen with GC alone on day 7. The absolute number of TCR alpha beta high MHC class Ihigh thymocytes after FK and GC was significantly lower than that of the control group, and was slightly lower than that after FK alone on day 14. These results suggest that combined treatment with FK506 and GC acts complexly to decrease rat CD4+8+ thymocytes and prevents thymocyte differentiation and maturation.
Animals↗
Flow cytometry analysis of increased expression of LFA-1/ICAM-1 in TCR-positive lymphocytes infiltrating cardiac allografts in rats.
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Animals↗
Identification of CD4- CD8- alpha beta T cells in the subarachnoid space of rats with experimental autoimmune encephalomyelitis. A possible route by which effector cells invade the lesions.
Experimental autoimmune encephalomyelitis (EAE) was induced in Lewis rats to elucidate the origin of effector T cells and the route by which they invade lesions. Since mouse studies have suggested that some autoimmune diseases are induced by extrathymic T cells in the liver, we focused our attention on the properties of mononuclear cells (MNC) isolated from the liver and other organs in rats with EAE. A small but significant proportion of LFA-1+ alpha beta T cells was identified in the liver as early as day 7 after immunization with myelin basic protein (MBP). Such LFA-1+ alpha beta T cells were also abundant among MNC attached to the spinal cord (i.e. subarachnoid space), and MNC infiltrated the spinal cord in rats with EAE (day 12). In electron microscopy, MNC attached to the spinal cord were found to be quite unique in terms of their large cell size with well-developed microvilli. More importantly, they were comprised of a considerably large proportion of double-negative CD4- CD8- T cells as well as single-positive CD4+ T cells. However, the cells which infiltrated the spinal cord were mainly CD4+. The present results raise the possibility that the subarachnoid space might be a major site for the expansion of extrathymic T cells in rats with EAE, and that only a limited population of CD4+ T cells invade the spinal cord directly through the outer layer and elicit EAE.
Animals↗
[How extensive should lymph node dissection be done for the surgery of the left lung cancer?].
Mediastinal lymph node dissection for cancer of the left lung is more difficult than for cancer of the right lung because of the presence of aorta. Location and frequency of lymph node metastasis were examined for 231 left lung cancer patients who underwent pulmonary resection and mediastinal lymph node dissection, and survival rate of them was evaluated. Subaortic (# 5), paraaortic (#6), subcarinal (#7), tracheobronchial (#4) lymph nodes were the most frequently involved N 2 nodes. 5-year survival rate of the patients who had #4, #5, #6, #7, #8 or #9 lymph node metastasis was 20.7%. #4, #5, #6, #7, #8 and #9 should be dissected for the surgery of the left lung cancer.
Carcinoma, Non-Small-Cell Lung↗
cDNA nucleotide sequence and primary structure of mouse uterine peptidylarginine deiminase. Detection of a 3'-untranslated nucleotide sequence common to the mRNA of transiently expressed genes and rapid turnover of this enzyme's mRNA in the estrous cycle.
Peptidylarginine deiminase is a protein-modulating enzyme which converts the arginine residues in proteins to citrulline residues. This study describes the complete primary structure of mouse peptidylarginine deiminase, which was deduced from nucleotide sequence analysis of cDNA clones plus proteochemical analysis of the purified enzyme. The composite cDNA sequence contained a 5' untranslated region of 7 bases, an open reading frame of 2019 bases that encoded 673 amino acids, a 3' untranslated region of 2662 bases, and part of a poly(A) tail. The N-terminal and C-terminal sequences of the enzyme matched the sequences deduced from nucleotide analysis. Furthermore, we determined that the N-terminal sequence was N alpha-acetyl-Met-Gln-, a sequence which has never previously been reported among N alpha-acetyl-Met proteins. The Arg 352 of the enzyme was converted to a citrulline residue and the potential Asn-linked glycosylation site (Asn542-Glu543-Ser544) had no carbohydrate moiety. Thus, mouse peptidylarginine deiminase consists of 673 amino acids with a molecular mass of 76,260. Mouse peptidylarginine deiminase mRNA has two AU-rich structures in the 3' untranslated region which exhibit a high degree of similarity to those in lymphokine, cytokine and proto-oncogene mRNA species. Since the rat enzyme (previously reported) does not possess these characteristic structures, we compared the levels of enzyme activity and mRNA in the mouse and rat uterus at four defined phases of the estrous cycle. The degradation of peptidylarginine deiminase and its mRNA proceeded significantly faster in the mouse than in the rat. We speculate that the unusual structure of the mouse enzyme and its mRNA be involved in this species-specific rapid degradation.
Amino Acid Sequence↗
Characterization of T cells infiltrating the heart in rats with experimental autoimmune myocarditis. Their similarity to extrathymic T cells in mice and the site of proliferation.
A model of experimental autoimmune myocarditis, which resembles fatal giant cell myocarditis in humans, was previously established in rats immunized by s.c. injection of human cardiac myosin. We characterized herein the surface phenotype of lymphocytes infiltrating the heart and pericardial cavity as well as of mononuclear cells in various organs by using mAb in conjunction with immunofluorescence tests. Since profound thymic atrophy always accompanied the diseased states, attention was focused on characterization of T cells with properties similar to those of extrathymic T cells. In mice, extrathymic T cells were activated in association with thymic atrophy, expressed high levels of LFA-1 and IL-2R beta-chains, and contained a significant proportion of double negative CD4-CD8- T cells. In diseased rats, a large proportion of activated T cells that expressed high levels of LFA-1 and IL-2R was demonstrated in the pericardial effusion and heart tissue. Such T cells were rare in the other organs. Light scatter and microscopic observation revealed that activated lymphoblasts were most abundant in the pericardial effusion. Moreover, one-fourth of such T cells in the pericardial effusion displayed double negative phenotype. These cells in rats might correspond to the extrathymic T cells in mice. However, only a limited population of such activated T cells infiltrated the heart tissue. Concerning the location of such T cells mainly in the outer layer of the heart, it raised the possibility that extrathymic T cell differentiation in these autoimmune rats might occur in the pericardial cavity, and the differentiated cells then migrated to the sites of the cardiac lesion.
Animals↗
Preferential distribution of V beta 8.2-positive T cells in the central nervous system of rats with myelin basic protein-induced autoimmune encephalomyelitis.
To determine the role of encephalitogenic T cells in the formation of lesions in the central nervous system (CNS), experimental autoimmune encephalomyelitis (EAE) was induced in Lewis rats by immunization with either myelin basic protein (MBP) or the synthetic peptide which corresponds to the 87-100 sequence of guinea pig MBP, and T cells expressing T cell receptor (TcR) V beta 8.2, V beta 8.5, V beta 10 and V beta 16 in the lymphoid organs and CNS were localized and quantified by flow cytometry (FCM) and immunohistochemistry. In normal rats, the percentage of T cells expressing these V beta phenotypes to the total number of TcR alpha beta+ T cells, as determined by FCM, ranged from 5% to 10% in the lymph node. V beta 16+ T cells were the most predominant population among the four V beta subsets tested. Essentially the same findings were obtained from the analysis of the lymphoid organs of rats with EAE which had been induced by immunization with the same two antigens. In sharp contrast, 15-20% of the T cells isolated from lesions of MBP-induced EAE expressed V beta 8.2. Thus, the percentage of V beta 8.2+ T cells in the EAE lesions was threefold higher than that in the lymph node, while the proportions of V beta 8.5+, V beta 10+ and V beta 16+ T cells were about the same in both organs. The predominance of V beta 8.2+ T cells in EAE lesions was confirmed by counts of immunohistochemically stained T cells in the spinal cord. Moreover, it was revealed that (i) the predominance of V beta 8.2+ T cells was greatest during the development of EAE and became less obvious at the recovery state, and (ii) at the peak stage of EAE, approximately 85% of V beta 8.2+ T cells were distributed in the parenchyma while 15% were in the perivascular space of the CNS vessels. These findings indicate that encephalitogenic T cells which express V beta 8.2 infiltrate the CNS at a very early stage of EAE and become the predominant population in infiltrating T cells, and further suggest that encephalitogenic T cells, not only recruit inflammatory cells in the CNS, but also cause neural tissue damage, such as demyelination.
Amino Acid Sequence↗
Characterization of intermediate TCR cells in the liver of mice with respect to their unique IL-2R expression.
We previously demonstrated that T cells with intermediate TCR intensity (i.e., intermediate TCR cells) which possibly generate extrathymically are preferentially present in the liver of mice. This population was further characterized with respect to the expression of IL-2 receptor (IL-2R) and others. Two-color staining for CD3 (or TCR alpha beta) and IL-2R alpha (and beta) demonstrated that intermediate TCR cells as well as NK cells constitutively expressed IL-2R beta but not IL-2R alpha. A small number of intermediate TCR cells was also identified in other immune organs by using this staining method. In vivo and in vitro stimulation experiments revealed that regular, bright TCR cells, which originally lacked the expression of both IL-2R alpha and beta, acquired the highest expression of IL-2R alpha and beta, while intermediate TCR cells did not. These results suggested, in conjunction with their other properties demonstrated here, that intermediate TCR cells might be more primitive T cells than regular T cells of thymic origin.
Animals↗
Thoracoscopic stapled bullectomy supported by suturing.
In 1985, a thoracoscopic technique for closing bullae with hemostatic clips was developed. However, the method was limited, and therefore clinical application was small. A linear endoscopic stapler (Endo-GIA) was developed in 1990. The advent of the Endo-GIA nearly made thoracoscopic treatment of spontaneous pneumothorax practicable, and ended the use of clipping. In addition, a new operative technique was developed, the 3-cm minithoracotomy bullectomy for the treatment of spontaneous pneumothorax. This technique has now become obsolete. The current method is that of a thoracoscopic stapled bullectomy using the Endo-GIA, supported by suturing. The recurrence rate was 2.7% (1/37) using this method. The one recurrence occurred in a case where no bullae were observed during the operation. Our findings suggest that thoracoscopic stapled bullectomy supported by suturing is a practicable treatment of spontaneous pneumothorax. An economical use of the endoscopic stapler and complementary suturing may be less expensive than using a laser. Pleurodesis should be performed in the patients in whom no distinct bullae are discovered thoracoscopically.
Humans↗
High frequency of etoposide (VP-16)-related secondary leukemia in children with non-Hodgkin's lymphoma.
PATIENTS AND METHODS: We report patients who were treated for non-Hodgkin's lymphoma (NHL) or Ki-1 antigen-positive (Ki-1) lymphoma with a T-8801 protocol that included etoposide (VP-16) and behenoylcytosine arabinoside. RESULTS: Secondary acute myeloid leukemia (AML) developed in 5 of 38 NHL and Ki-1 lymphoma patients, and the cumulative risk at 4 years was 18.4%. The median time from the initiation of the chemotherapy to the development of AML was 21 months (range, 13-30). Four patients had a FAB M5 morphology, and one had FAB M2. In four of five examined cases, chromosomal alterations involving the long arm of chromosome 11 were demonstrated at the time of development of AML. None of the 46 NHL patients who we treated with another protocol (B-8801), using significantly higher cumulative doses of VP-16 than in the case of the patients with T-8801 and a different schedule of VP-16 administration, developed secondary AML. CONCLUSIONS: The risk of secondary AML possibly related to the use of VP-16 given twice weekly.
Adolescent↗
Radioresistance of intermediate TCR cells and their localization in the body of mice revealed by irradiation.
Extrathymic generation of T cells in the liver and in the intestine was recently demonstrated. We investigated herein whether such T cells, especially those in the liver, are present in other organs of mice. This investigation is possible employing our recently introduced method with which even a minor proportion of extrathymic, intermediate TCR cells in organs other than the liver can be identified. Intermediate TCR cells expressed higher levels of IL-2R beta and LFA-1 than bright TCR cells (i.e., T cells of thymic origin) as revealed by two-color staining. Although intermediate TCR cells were present at a small proportion in the spleen and thymus, they predominated in these organs after irradiation (9 Gy) and bone marrow reconstitution, or after low dose irradiation (6 Gy). This was due to that intermediate TCR cells were relatively radioresistant, whereas bright TCR cells were radiosensitive. Microscopic observation and immunochemical staining showed that intermediate TCR cells in the spleen localized in the red pulp and those in the thymus localized in the medulla. These intermediate TCR cells displayed a large light scatter, similar to such cells in the liver. The present results suggest that intermediate TCR cells may proliferate at multiple sites in the body.
Animals↗
Epstein-Barr virus-infected T lymphocytes in Epstein-Barr virus-associated hemophagocytic syndrome.
The clonal composition of EBV-infected cells was examined in three cases of EBV-associated hemophagocytic syndrome by analysis of the heterogeneity of terminal repetitive sequences in the EBV genome, indicating monoclonal expansion of EBV-infected cells in all cases. Involvement of T lymphoid cells was determined by in situ hybridization using 35S-labeled RNA probes specific for the small EBV-encoded nuclear RNAs, EBER1 and EBER2, in combination with immunostaining for the TCR-beta chain, CD45RO, CD20, CD30 and CD68 antigens in these three cases. The majority of lymphoid cells showing EBER transcripts were stained by antibodies against CD45RO and T cell receptor-beta. In contrast, EBER-specific signals were not detectable on B cells or hemophagocytic cells. These data support the concept that EBV-associated T cell proliferation is a primary feature of EBV-AHS.
Adolescent↗
In situ inactivation of infiltrating T cells in the central nervous system with autoimmune encephalomyelitis. The role of astrocytes.
Our previous study using bromodeoxyuridine (BrdU) has shown that T cells in lesions of experimental autoimmune encephalomyelitis (EAE) in the rat central nervous system (CNS) lose their proliferating capability immediately after infiltration into the CNS. To characterize the nature of this phenomenon in more detail, we have isolated T cells from EAE lesions and examined their surface phenotype and response to encephalitogenic antigen, myelin basic protein (MBP). By flow cytometry (FCM) analysis, it was revealed that compared with peripheral blood lymphocytes, up-regulation of interleukin-2 (IL-2) receptors (0.06%-->3.73%) and the lymphocyte function-associated antigen-1 (LFA-1) molecules (0.76%-->17.6%) on spinal cord T cells (SCT) was observed. In spite of the latter finding suggesting that SCT are activated, SCT recovered from rats with full-blown EAE responded very poorly to MBP. The addition of thymocytes or thymocytes plus astrocytes did not alter the low responsiveness of SCT. More importantly, astrocytes strongly suppressed the response of lymph node T cells to MBP. Using MBP-specific T-line cells, it was revealed that T-cell suppression might be induced by incomplete presentation of MBP and release of suppressive humoral factors by astrocytes. Since the response of SCT was still poor when assayed after three and 12 rounds of stimulation with the antigen and propagation with IL-2, this phenomenon is long lasting. These findings are consistent with the findings obtained by the BrdU study that infiltrating T cells into the CNS do not proliferate vigorously. Taken together, the poor response of infiltrating T cells to MBP would be induced by co-existing cells such as astrocytes although the T cells are in an active form as judged by their surface phenotype. The present study suggests that activation of non-haematopoietic parenchymal cells in each organ by infiltrating T cells and subsequent inactivation of the T cells are important healing processes for organ-specific autoimmune diseases.
Animals↗