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Biomedical subjects

T Tabira

Publications and source records attributed to T Tabira.

At least 127 records · Page 7Linked to original sources
PubMed1990

HLA-DP beta and susceptibility to multiple sclerosis: an analysis of caucasoid and Japanese patient populations.

Nonradioactive sequence-specific oligonucleotide (SSO) probes specific for the HLA-DP beta locus have been used in a simple dot-blot assay to DP beta-type samples amplified by the polymerase chain reaction (pcr) from Caucasoid (n = 24) and Japanese (n = 23) patients with multiple sclerosis (ms) as well as ethnically matched controls. In contrast to previous reports, no DP beta allele was found to be increased in either patient population. However, the results do show a dramatic difference in the allele frequencies between the two control populations, further emphasizing the need for ethnically matched controls in studies of HLA and disease.

Alleles↗
PubMed1990

Interleukin 3 as a trophic factor for central cholinergic neurons in vitro and in vivo.

We have found that interleukin 3 (IL-3), a growth factor for hematopoietic cells, is a novel trophic factor for mouse and rat central cholinergic neurons. It enhanced neurite outgrowth and elevated choline acetyltransferase activity. The effect seems to be specific for cholinergic neurons, since somatostatin release and glutamic acid decarboxylase and 2',3'-cyclic nucleotide 3'-phosphodiesterase activities were not significantly influenced by IL-3. In vivo, IL-3 was infused into the lateral ventricles of rats after unilateral axotomy of the septohippocampal pathways. Two weeks later, the IL-3-treated animals showed significant numbers of acetylcholinesterase-positive neurons remaining in the septal region.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1990

Developmental and aging changes in the expression patterns of beta-amyloid in the brains of normal and Down syndrome cases.

Immunohistochemical staining with polyclonal antibodies to synthetic amyloid (residues 1-28 of A4) was performed on normal and Down syndrome brains from fetuses to adults. Positive staining appeared in the cytoplasmic processes of astrocytes in the subpial layer and white matter of developing brains, and reappeared in astrocytic fibers of the subpial layer as well as in cerebrovascular and plaque core amyloid in elderly brains. The reappearance of positively stained astrocytes and amyloid occurred earlier in adult Down syndrome patients. The results indicate that the A4 protein is a developmental protein, and its reappearance in Alzheimer and adult Down syndrome brains may be related to the regeneration process.

Adolescent↗
PubMed1990

Susceptibility to proteolipid apoprotein and its encephalitogenic determinants in mice.

We investigated in mice strain differences in induction of experimental allergic encephalomyelitis by proteolipid apoprotein and studied encephalitogenic determinants. SJL/J, C3H/He, CBA/J and A/J mice were high responders, BALB/c and AKR/J mice were moderately susceptible, and DBA/2, B6 and congenic strains of B10 background were low responders. Synthetic peptide 136-150 was encephalitogenic for SJL/J mice, and 215-232 was encephalitogenic for C3H/He mice. These encephalitogenic derterminants are present in the extracellular portion of proteolipid apoprotein in myelin.

Animals↗
PubMed1990

Effect of thymic hormones on induction of experimental allergic encephalomyelitis in old mice.

This study was aimed at restoring decreased T-cell functions and reduced susceptibility to proteolipid apoprotein (PLP) induced-experimental allergic encephalomyelitis (EAE) in old mice with thymic hormones. Thymosin fraction 5 (TF-5) and serum thymic factor (FTS) had no significant in vitro and in vivo effect on proliferative responses to PLP and concanavalin A (Con A), and on EAE induction in young and old mice. These results suggest that decreased T-cell functions cannot be restored by these thymic hormones tested.

Aging↗
PubMed1990

Autoproliferative and self-reactive T-cell lines from patients with HTLV-I-associated myelopathy.

In two patients with human T lymphotropic virus type 1 (HTLV-I)-associated myelopathy (HAM) and a non-HAM HTLV-I carrier, T-cell lines were generated and characterized from cerebrospinal fluid (CSF) lymphocytes and peripheral blood lymphocytes (PBL). In total, 62 T-cell lines were established using direct plating technique for expanding human T lymphocytes. Sixty three percent of the T-cell lines were CD4+, CDw29+ and HTLV-I gag+. CD8+T-cell lines were also established and they were gag-. Proliferation in the absence of additional antigens and exogenous interleukin 2 ("autoproliferation") was observed in 61% of the T-cell lines and significantly correlated with HTLV-I antigen (gag) expression. In addition, some T-cell lines from HAM patients exhibited proliferative response to self PBL, and the magnitude of their responses was diverse according to the phenotypes of stimulating cells. Therefore, the spontaneous lymphoproliferation observed in patients with HAM is generated by three components; HTLV-I-infected T cells and T cells reactive against HTLV-I and against self antigens. Since most gag+ T-cell lines produced lymphotoxin (LT)/tumor necrosis factor alpha (TNF alpha), it is suggested that those T cells are playing important roles in the pathogenesis of HAM.

Cell Line↗
PubMed1989

Putative N-terminal splitting enzyme of amyloid A4 peptides is the multicatalytic proteinase, ingensin, which is widely distributed in mammalian cells.

The main characteristic changes observed in Alzheimer's disease (AD) are the presence of neurofibrillary tangles and the deposition of amyloid A4 peptides. The most abundant amyloid A4 peptide species in AD (which we tentatively named A4') is composed of 39 amino acids, which is devoid of the 3 N-terminal amino acids, Asp-Ala-Glu, of the originally reported A4 peptide. We synthesized a model peptide substrate, Suc-Ala-Glu-methylcoumarinamide (MCA), to identify the proteinase that splits the A4' peptide. DEAE-cellulose column chromatography of rat liver and porcine brain extracts showed that only one peak material digested the synthetic substrate at pH 8. The results for the final preparation indicate that the Suc-Ala-Glu-MCA-degrading enzyme is a high-molecular-mass proteinase, with a molecular mass of above 500,000, and is composed of several low-molecular-mass subunits. These results suggest that a non-lysosomal multicatalytic proteinase (we named this enzyme ingensin (ingens = large in Latin). Ishiura, S. et al. (1985) FEBS Lett. 189, 119-123) catalyzes the above reaction. Antiserum against the purified multicatalytic proteinase, ingensin, crossreacted with the purified Suc-Ala-Glu-MCA-degrading proteinase. It is likely that ingensin shows a similar action toward amyloid precursor protein (APP) in vivo.

Amino Acid Sequence↗
PubMed1989

Semple rabies vaccine: presence of myelin basic protein and proteolipid protein and its activity in experimental allergic encephalomyelitis.

Myelin basic protein (MBP) as a cause of postvaccinal encephalomyelitis (PVE) due to Semple rabies vaccine (SRV) has been suggested in previous reports. No actual measurement of MBP in SRV was done. In this study we detected MBP and PLP in the vaccine using immunological methods. The vaccine was found to contain 28 micrograms MBP per ml vaccine. Inoculation with SRV plus adjuvant resulted in the development of experimental allergic encephalomyelitis (EAE) in 2 of 3 guinea pigs. For control, chick embryo vaccine (CEV) was used and MBP was not detected. EAE was not induced in animals inoculated with it. These results suggest that MBP in vaccines may play a decisive role in the production of PVE.

Animals↗
PubMed1989

Abrogation of spleen macrophage suppressive activity by 15-deoxyspergualin.

We studied the immunomodulatory mechanism of 15-deoxyspergualin (DSG), a novel antitumor agent. To assess this, we used a mixed culture of antigen-primed lymph node cells (LNC) and spleen cells (SPC). In normal or untreated conditions, SPC suppressed the proliferative response of LNC to the antigens. In contrast, SPC from DSG-treated animals did not show any suppressive activity. This suppression was mediated by adherent cells in SPC but the suppression mechanism was recovered when DSG-treated spleen macrophages were reconstituted with control spleen nonadherent cells. These data suggest that DSG abrogates nonspecific suppressive activity of spleen cells by acting on both adherent and nonadherent cells.

Animals↗
PubMed1989

Cellular and molecular aspects of the pathomechanism and therapy of murine experimental allergic encephalomyelitis.

Experimental allergic encephalomyelitis (EAE) is an autoimmune disease of the central nervous system (CNS). Its immune mechanism is well understood at the cellular and molecular levels, which is herein reviewed. Susceptibility to EAE is under the control of the genes partially inside and partially outside the H-2 complex. There are two myelin constituents known to be encephalitogenic, myelin basic protein and proteolipid apoprotein. EAE is mediated by effector T cells sensitized to the encephalitogen. Effector T cells bear surface phenotypes of Lyt1+2-, L3T4+, and they are activated by the encephalitogen/self Ia complex or certain alloantigens and acquire encephalitogenic activity. By unknown homing mechanisms, the effector T cells invade the CNS and induce the target phase phenomena, which include Ia-antigen expression in the local tissue, activation of procoagulant activity, breakdown of the blood-brain barrier, and excretion of lymphokines which induce inflammation and demyelination, resulting in functional alteration. Possibility of specific immune therapy is postulated as a model for human autoimmune disease.

Animals↗
PubMed1988

Immunohistochemical study of Alzheimer's disease using antibodies to synthetic amyloid and fibronectin.

Etiology and source of amyloid deposition in senile plaques of Alzheimer's disease (AD) are still unknown. In order to know whether or not fibronectin (Fn), an adhesive glycoprotein, is related to the amyloid deposition in the senile plaque, we conducted immunohistochemical studies using polyclonal anti-Fn and affinity-purified anti-amyloid component (Affi 28). Affi 28 was made by immunizing a rabbit against the synthetic peptide corresponding to residues 1-28 of the amyloid core protein reported by Masters et al. (1985). According to this study, four points became clear. First, Affi 28 is able to stain the subpial regions of AD as well as cerebrovascular amyloid and amyloid plaque cores. Second, it is suggested either that the etiology and source of neurofibrillary tangles and Pick body is distinct from that of the senile plaque or that any Affi 28 determinants of neurofibrillary tangles and Pick body are obscured sterically. Third, Affi 28 is useful to distinguish the senile plaque from the amyloid plaque of Creutzfeldt-Jakob disease. Last, there is no association between the amyloid in the senile plaque and Fn, at least immunohistochemically. The absence of Fn in the senile plaque suggests that Fn may not be requested for the deposition of amyloid fibrils.

Alzheimer Disease↗
PubMed1988

In vivo and in vitro studies of the prevention of proteolipid apoprotein-induced murine experimental allergic encephalomyelitis by monoclonal antibody against L3T4.

The suppressive effect of anti-L3T4 monoclonal antibody (mAb) on murine experimental allergic encephalomyelitis (EAE) induced by sensitization with proteolipid apoprotein (PLP) was examined in vivo and in vitro. This mAb inhibited the antigen-specific proliferation of the encephalitogenic T cell lines but did not block the mitogen-mediated response. Serial injections of the mAb during the pre-effector phase of EAE markedly suppressed the development and relapse of the disease but this treatment initiated after appearance of clinical signs was not effective. In treated animals, L3T4+ T cells in the spleen were profoundly decreased and the antigen-specific proliferative response of spleen cells was completely suppressed. Moreover, adoptive transfer of spleen cells from the treated mice induced resistance against EAE induction in the recipients. However, no obvious evidence for antigen-specific suppressor cells was found in vitro in the L3T4- populations of spleen cells from treated mice.

Acute Disease↗
PubMed1988

Absence of antibodies to HTLV-1 in sera from Hungarian MS patients.

The aim of this study is to examine the association between multiple sclerosis (MS) and anti-human T-lymphotropic virus type I (HTLV-I) antibody. Serum samples from 16 Hungarian caucasians with MS, 2 gipsy patients with MS, 13 Hungarian caucasians with other neurological diseases (OND) and 2 gipsy patients with OND were tested by Western blot combined with autoradiography using disrupted virus from MT-2 cell line and recombinant p24 as antigens. Negative results were obtained in all samples except for 3 Hungarian OND which were reactive to disrupted virus, but not to recombinant p24.

Adult↗
PubMed1988

Autoimmune demyelination in the central nervous system.

Autoimmune demyelination was studied in EAE induced by active challenge or by transfer of effector T-cell lines or clones specific for myelin basic protein or proteolipid apoprotein. The following points became clear: (1) Proteolipid apoprotein is responsible for widespread demyelination; (2) demyelination is more significant in EAE with a more chronic disease process; (3) a single T-cell clone can mediate significant demyelination without the aid of recipient-derived T-cell populations; (4) the difference in vulnerability between axons and myelin may account for the T-cell-mediated demyelination; and (5) effector T-cell clones can be activated by allogeneic antigens.

Animals↗
PubMed1987

Experimental allergic encephalomyelitis mediated by murine encephalitogenic T cell lines specific for myelin proteolipid apoprotein.

T cell lines specific for bovine myelin proteolipid apoprotein (PLP) were established from SJL/J mice. The line cells bore surface phenotypes of T helper/inducer cells (Lyt-1+, Lyt-2-, L3T4+) and responded well to bovine, rat, and guinea pig PLP but not to myelin basic protein. One line responded to major PLP, and another responded to both major PLP and DM-20, which are the two major intrinsic membrane proteins of the central nervous system (CNS) myelin. Intraperitoneal inoculation of 4 to 30 X 10(6) PLP-activated line cells followed by injection of pertussis vaccine induced acute inflammatory disease of the CNS, with typical clinical signs of EAE mostly in a week in recipient mice that had been treated with low-dose irradiation. Almost all animals recovered completely, and two of the 12 animals relapsed 42 or 75 days after inoculation. The lesions were restricted to the CNS and were characterized by perivascular and parenchymal infiltration of inflammatory cells, fibrin deposit, and demyelination. In the severe lesions, axons were also damaged. These observations suggest that PLP is a definite encephalitogen, and PLP-sensitized effector T cells induce inflammatory demyelination in the CNS.

Animals↗
PubMed1987

Recognition of alloantigens and induction of experimental allergic encephalomyelitis by a murine encephalitogenic T cell clone.

In this communication we report a SJL/J (H-2s, Mlsc)-derived encephalitogenic T cell clone 4b.14a which has dual specificities for myelin basic protein/I-As and allogeneic H-2Ik gene products. Monoclonal antibodies specific for public class II major histocompatibility complex (MHC) determinants (Ia.17, I-Ak, r and Ia.7) and anti-L3T4 antibody inhibited the response of the clone 4b.14a to alloantigens, but a monoclonal antibody specific for a private determinant on I-Ak (Ia.2) did not inhibit the response. Although this clone proliferated in response to allogeneic spleen cells expressing H-2Ik determinants regardless of disparate Mlsa, b, c, d alleles, CBA/N cells (H-2k, Mlsnull) failed to stimulate the clone 4b.14a. These results suggest that recognition of allogeneic class II MHC molecules by this clone requires recognition with non-MHC gene products such as Mls. In addition, the clone 4b.14a stimulated by alloantigens could mediate clinical signs of experimental allergic encephalomyelitis in syngeneic recipients. However, interleukin 2 of rat spleen cell origin alone failed to activate the clone cells to make them encephalitogenic, though it could make them proliferate. The significance of these findings for T cell recognition and activation is discussed.

Animals↗