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T Abo

Publications and source records attributed to T Abo.

At least 109 records · Page 6Linked to original sources
PubMed1997

Identification of nicotinic acetylcholine receptors on lymphocytes in the periphery as well as thymus in mice.

The existence of nicotinic acetylcholine receptors (nAChR) on lymphocytes remains controversial. We attempted to show the existence of nAChR on murine lymphocytes. The intraperitoneal injection of nicotine induced the lymphocytosis in the spleen on day 3. Although freshly isolated lymphocytes bound small quantities of fluorescein isothiocyanate (FITC)-conjugated alpha-bungarotoxin (alpha BuTx), they began to bind alpha BuTx after incubation in medium. In contrast to granulocytes, various lymphocyte subsets obtained from various lymphoid organs were found to bind alpha BuTx. Affinity purification of alpha BuTx-binding protein revealed that lymphocytes expressed the same nAChR molecules as those of muscle. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis showed that lymphocytes expressed the alpha-subunit mRNA of nAChR. These results suggest that lymphocytes carry nAChR on the surface and are stimulated directly via their nAChR by parasympathetic nerve stimuli.

Animals↗
PubMed1997

Neonatal granulocytosis is a postpartum event which is seen in the liver as well as in the blood.

In a recent series of studies, we demonstrated that stress in humans and animals, with resultant sympathetic nerve strain, induces severe granulocytosis, because granulocytes carry adrenergic receptors on the surface. Because activated granulocytes produce free radicals and superoxides, they sometimes induce tissue damage if the stress is too strong or continuous. Human neonates are also known to show high levels of granulocytes in the peripheral blood. In this study, we investigated whether such neonatal granulocytosis are a stress-associated response at birth. Both human and mouse materials, before and after birth, were used. The number of leukocytes in the blood, as well as some other factors in the serum, were measured. Although levels of granulocytes were found to be low in fetal humans and mice, they increased sharply after birth. In parallel with this postpartal granulocytosis, transaminases in sera increased transiently. In reference to results of a transient elevation in the levels of catecholamines at birth in mice, all these phenomena resemble stress-associated responses. Indeed, fatty liver and hematopoietic destruction in the liver were also observed in mice and humans. At this time, the production of inducible nitric oxide synthase (iNOS) by granulocytes in the liver was evident. These results suggest that neonatal granulocytosis is a postpartum event which results from various stresses (e.g., oxygen stress) at birth. This event may be responsible for such well-known neonatal phenomena as the termination of fetal hematopoiesis in the liver and as neonatal jaundice.

Alanine Transaminase↗
PubMed1997

IgA nephropathy-specific expression of the IgA Fc receptors (CD89) on blood phagocytic cells.

We analysed the biochemical features of receptors for the Fc-region of IgA (Fc alphaR, CD89) on blood monocytes and granulocytes of patients with IgA nephropathy (IgAN). Fc alphaR on monocytes of IgAN were found to have a higher Mr (60-80 kD) than those of control monocytes (50-75 kD) and granulocytes (55-75 kD) in both IgAN and controls as shown by immunoprecipitation analysis. Removal of N-linked carbohydrates from Fc alphaR on monocytes of IgAN revealed a 32-36 kD protein core, the Mr of which was still higher than that of controls (28-32 kD). When Fc alphaR transcripts were analysed by reverse-transcription-PCR, only one prominent band was visualized in PCR products from IgAN monocytes. Since the results thus far show that IgAN monocytes express Fc alphaR protein and mRNA differently from granulocytes and control monocytes, PCR products were then cloned and sequenced. The predominant band in PCR products from IgAN monocytes was identical to that of the Fc alphaR a.1 transcript, and an additional 10 transcripts containing five novel transcripts were obtained from granulocytes and control monocytes. In three transcripts, we found an insertion sequence between the S2 and EC1 domains, suggesting the existence of a new exon. These results suggest a predominant usage of Fc alphaR a.1 among various transcripts of Fc alphaR in IgAN monocytes.

Adolescent↗
PubMed1997

Effect of cardiopulmonary bypass on cytokine release and adhesion molecule expression in alveolar macrophages. Preliminary report in six cases.

Although recent studies have shown that adhesion molecules on alveolar macrophages are important in a variety of pulmonary diseases, there have been few studies on the phenotypic and functional changes of alveolar macrophages during cardiopulmonary bypass. To investigate the possible role of alveolar macrophages in activating pulmonary immunity during cardiopulmonary bypass, we measured the expression of adhesion molecules on alveolar macrophages and peripheral blood monocytes in patients undergoing cardiopulmonary bypass. Antigens were stained with monoclonal antibodies against adhesion molecules, and the expression of antigens was quantified by flow cytometry as the ratio of specific to nonspecific linear fluorescence. On alveolar macrophages obtained after the release of aortic cross-clamp, macrophages as compared with alveolar macrophages obtained before cardiopulmonary bypass, there was a significant enhancement of CD11a, CD11b, CD11c, and CD18. In addition, alveolar macrophages, but not peripheral monocytes, produced higher levels of TNF-alpha and IL-8 when they were cultured in vitro. A higher expression of CD11 and CD18 on alveolar macrophages and enhanced production of cytokines after release of the aortic cross-clamp may contribute to immune activation in lung by macrophage-lymphocyte interaction.

Adult↗
PubMed1997

[Immune system and diseases that vary with circumstance and physical condition].

Empirically we all know that our immune system varies depending on environmental factors and physical conditions. However, such recognition has remained at an empirical level for a long time without the accumulation of scientific data. The major reason is that the substance and its receptor that connect physical conditions with the immune system have previously been obscure. Adrenergic and cholinergic receptors on leukocytes may be important in understanding that relationship. Furthermore, we have to consider the mutually antagonistic functions of granulocytes and lymphocytes in the body. All stimuli from environmental factors change our physical conditions and subsequent changes in the autonomic nervous system influence our immune system through adrenergic receptors on granulocytes and cholinergic receptors on lymphocytes. Overactivation of granulocytes induces purulent diseases or tissue destruction, whereas overactivation of lymphocytes induces allergic diseases.

Animals↗
PubMed1996

Extrathymic differentiation of resident T cells in the joints of mice with collagen-induced arthritis.

Murine collagen-induced arthritis (CIA) is known as a T cell-mediated autoimmune disease, although autoantibodies are also suspected to be associated with the onset of the disease. To determine the origin of such T cells in the joints of mice with CIA, their phenotypic properties as well as those of T cells in other immune organs were examined in DBA/1 mice. Since a significant number of mononuclear cells (MNC) was also yielded by the joints of normal DBA/1 mice, the properties of these T cells were examined in parallel. When CIA was induced by an intradermal injection of type II collagen at the base of the tail, the numbers of MNC yielded by the regional lymph nodes and the foot joints were doubled. Interestingly, regardless of the onset of CIA, the joints were always comprised of unique T cell populations, including IL-2(R)alpha- beta+ T cells, gammadelta T cells, CD8alpha+ beta- cells, and CD44+ L-selectin- cells. All these properties coincide with those of extrathymic T cells in liver and intestine. In the case of gammadelta T cells in joints, Vgamma and Vdelta usages were unique and different from those in the other organs. More importantly, Vgamma and Vdelta usages in gammadelta T cells in the joints of normal mice and in those of mice with CIA were essentially the same. Taken together with the expression of recombination-activating gene-1 and -2 mRNAs by MNC in mice with CIA, these findings raise the possibility that the joints have their own resident T cells that are extrathymically generated in situ.

Animals↗
PubMed1996

Simultaneous activation of granulocytes and extrathymic T cells in number and function by excessive administration of nonsteroidal anti-inflammatory drugs.

Nonsteroidal anti-inflammatory drugs (NSAIDs) sometimes show serious side effects such as damage to the gastroduodenal mucosa and dysfunction of the liver. Although many investigators have focused on some types of leukocytes, a comprehensive study concerning all types of leukocytes, especially recently identified extrathymic T cells, remains to be done. When mice were treated with an intraperitoneal injection of indomethacin (50 or 300 microg/mouse), the number of thymocytes decreased while the number of MNC in various peripheral organs increased. This increase in MNC was due mainly to the increase in the numbers of granulocytes and extrathymic T cells. Reflecting thymic atrophy, the proportion of thymus-derived T cells distributed in the periphery decreased. The use of other NSAIDs revealed that granulocytosis seen in the periphery arose from a selective activation of myelomonocytic cells in the bone marrow. Some functional experiments using the Ca2+ influx, iNOS mRNA expression, and autoreactive cytotoxicity as indicators suggested that granulocytes and extrathymic T cells were in activated states not only in number but also in function. Since both granulocytes and extrathymic T cells become cytotoxic effectors against self-tissues or self-cells when overactivated, these activated leukocytes may be intimately related to the etiology of the tissue damage inducible by NSAIDs (i.e., adverse drug reaction).

Animals↗
PubMed1996

Level of myelopoiesis in the bone marrow is influenced by intestinal flora.

Mice were orally given kanamycin (50 mg/day/ mouse) for 1 or 2 weeks. Almost all bacteria in the intestine were eliminated within a week. In parallel with this elimination, the level of granulocytes in the bone marrow decreased from 41 to 31%. Since the total number of bone marrow cells decreased as well (up to one-third), the decrease in the level of granulocyte generation in the bone marrow was substantial. Kanamycin is not absorbed from the intestine into the body; namely, it does not have a direct effect on the bone marrow. It is speculated that the interaction of granulocytes or epithelial cells with intestinal bacteria accelerates the production of free radicals and superoxids, some cytokines, or unknown factors and that such substances then stimulate the generation of granulocytes in the bone marrow. The present results suggest that intestinal flora and other resident bacteria are important for maintaining the level of myelopoiesis in the bone marrow.

Animals↗
PubMed1996

Activation by estrogen of the number and function of forbidden T-cell clones in intermediate T-cell receptor cells.

When estrogen (1 mg/mouse) was subcutaneously administered once into mice, the number of liver MNC increased but the number of thymocytes decreased profoundly from Day 3 to Day 20. Phenotypic characterization revealed that the proportion of intermediate (int) TCR cells with IL-2 receptor beta-chain (IL-2R beta) was elevated in both the liver and the thymus. Attention was then focused on how forbidden clones were distributed among various T-cell subsets, including IL-2R beta+ int TCR cells and IL-2R beta-high TCR cells. IL-2R beta+ int TCR cells are generated through the extrathymic pathway in the liver and an alternative intrathymic pathway, whereas IL-2R beta- high TCR cells are generated through the mainstream of T-cell differentiation in the thymus. It was demonstrated that forbidden clones, V beta 3+ and V beta 11+ cells, in BALB/C mice (Mls-1b2a) were confined to IL-2R beta+ int TCR cells, irrespective of the administration of estrogen. Interestingly, the proportion of forbidden clones among int TCR cells increased in the liver but decreased in the thymus after the administration of estrogen. Liver MNC that contained a high level of forbidden clones showed unexpected high levels of spontaneous proliferation and of the proliferative response to immobilized anti-V beta mAb (even in the combination of forbidden clone stimulations). The present results reveal that the levels of both int TCR cells and forbidden clones that induce hepatocyte damage preferentially increase in the liver, one of the prime target organs in autoimmune diseases, when estrogen is administered.

Animals↗
PubMed1996

Physiological dose of estrogen regulates extrathymic T cells in female mice.

Bilateral ovariectomy was performed in female C57BL/6 mice to investigate whether extrathymic T cells in the liver are regulated by physiological doses of estrogen or progesterone. Extrathymic T cells were identified using a two-color immunofluorescence test for CD3 and interleukin-2 receptor beta-chain (IL-2R beta) antigens. The T cells were identified as intermediate CD3+ cells with a high expression of IL-2R beta. It was further demonstrated that the proportion and number of intermediate CD3+ cells decreased in response to ovariectomy, an effect that was countered by estrogen administration. These results suggest that the activation of extrathymic T cells may be regulated by physiological levels of estrogen.

Animals↗
PubMed1996

c-kit+ stem cells and thymocyte precursors in the livers of adult mice.

Livers of the adult mice contain c-kit+ stem cells that can reconstitute thymocytes, multiple lineage cells, and bone marrow (BM) stem cells. Transfer of 1 x 10(7) hepatic mononuclear cells (MNC) and 5 x 10(4) hepatic c-kit+ cells of BALB/c mice induced DP thymocytes within a week in four Gy-irradiated CB17/-SCID mice, but 2 wk were required for BM cells or BM c-kit+ cells to produce DP thymocytes. Moreover, B cell-depleted BM cells or liver MNC of SCID mice that had been rescued by hepatic MNC of BALB/c mice again reconstituted thymus and B cells of other irradiated SCID mice. CD3- IL-2R beta- populations of both BM cells and hepatic MNC of C57BL/6 (B6) mice could generate T cells with intermediate TCR (mostly NK1.1-) in the liver of irradiated B6 SCID mice before thymic reconstitution (extrathymic T cells). Furthermore, transfer of liver c-kit+ cells of B6-Ly 5.1 mice into irradiated B6 SCID (Ly5.2) mice revealed that liver c-kit+ cells can reconstitute myeloid and erythroid lineage cells. These results strongly suggest that the liver contains pluripotent stem cells and serves an important hematopoietic organ even into adulthood.

Animals↗
PubMed1996

A comparison of proliferative response to IL-7 and expression of IL-7 receptors in intermediate TCR cells of the liver, spleen, and thymus.

It is well established that IL-7 supports the earliest differentiation of both T and B cells in fetal and adult life. On the other hand, mature lymphocyte subsets tend to decrease the response to IL-7 in case of T and B cells. In a recent study, NK1.1+ T cells in the thymus are also found to efficiently respond to IL-7 and express IL-7 receptors (IL-7R). This population is generated through an alternative intrathymic pathway. A similar population, namely, T cells with intermediate levels of TCR (i.e., int TCR cells) are known to be generated through extrathymic pathways. In this respect, the proliferative response to IL-7 and the expression of IL-7R in int TCR cells of various organs were compared. Whole liver MNC and isolated int TCR cells from the liver were found to proliferate in response to IL-7. Moreover, a considerable population of int TCR cells in both the liver and thymus were found to carry a higher density of IL-7R on the surfaces than high TCR cells. More precisely, the intensity of IL-7R on int TCR cells in the thymus was the highest but those on int TCR cells in other organs were slightly lower (i.e., int TCR cells in the thymus greater than int TCR cells in the liver greater than high TCR cells). Taken together with the result of expression of IL-7 mRNA by hepatocytes and thymic tissues, it is concluded that IL-7 is one of the most important growth factors for int TCR cells both in the liver and thymus.

Animals↗
PubMed1996

Characterization of CD4-CD8- T cell receptor alpha beta + T cells appearing in the subarachnoid space of rats with autoimmune encephalomyelitis.

Inflammation of the central nervous system (CNS) in experimental autoimmune encephalomyelitis (EAE) starts in the subarachnoid space (SAS) and spreads later to the adjacent CNS parenchyma. To characterize the nature of lesion-forming T cells in situ in more detail, T cells were isolated from the SAS and their surface phenotype and the nucleotide sequence of the junctional region of the T cell receptor (TCR) was determined and compared with those of the lymph node (LN) and spinal cord (SC) T cells. Characteristically, more than 70% of SAS TCR alpha beta + T cells isolated at the early stage of EAE lacked both CD4 and CD8 molecules, whereas those from LN and SC were either CD4+ or CD8+. Analysis of nucleotide sequences of the junctional region of TCR revealed that T cells bearing a sequence identical to that for encephalitogenic T cell clones were found in both SAS and SC. Furthermore, purified CD4-CD8- T cells expressed CD4 molecules after culture. At the same time, these T cells acquired reactivity to myelin basic protein and induced passive EAE in naive animals after adoptive transfer. Our results suggest that CD4-CD8- T cells in the SAS are precursors of lesion-forming T cells in the SC and that phenotype switching takes place during the process of T cell infiltration into the CNS parenchyma. The double-negative nature of these T cells may explain an escape of encephalitogenic T cells from negative selection in T cell differentiation.

Amino Acid Sequence↗
PubMed1996

Existence of a small population of IL-2R beta hi TCRint cells in SCG and MRL-lpr/lpr mice which produce normal Fas mRNA and Fas molecules from the lpr gene.

Mice carrying the lpr gene, SCG and MRL-lpr/lpr mice, were used to characterize the phenotype and lpr gene of abnormally proliferating T cells in these mice. A major population which expanded in these mice were T cells expressing intermediate (int) levels of T cell receptor (TCR) (and CD3) and the phenotype of interleukin-2 receptor (IL-2R) beta lo alpha- (possibly abnormal TCRint cells). The levels of TCRhi cells of thymic origin (generated through the mainstream of T cell differentiation in the thymus) profoundly decreased after the onset of disease. However, a small population of normal TCRint cells (i.e. IL-2R beta hi alpha-) were also found to exist in all tested organs. For example, the majority of abnormal IL-2R beta lo TCRint cells were CD4-8- CD2-, while normal IL-2R beta hi TCRint cells were a mixture of single-positive cells (mainly CD8+), CD4-8- cells and CD2+ cells. Moreover, normal TCRint cells preferentially produced normal Fas mRNA and Fas molecules from the lpr gene. This phenomenon explains the leaky appearance of normal Fas mRNA and Fas molecules in mice carrying the lpr gene. It is suggested that a small population of IL-2R beta hi TCRint cells are resistant to the lpr genetic abnormality.

Animals↗
PubMed1996

Restricted appearance of self-reactive clones into T cell receptor intermediate cells in neonatally thymectomized mice with autoimmune disease.

Neonatally thymectomized (NTx) mice fall victim to such autoimmune diseases as gastritis and pancreatitis with aging. Self-reactive T cell clones are known to be consistently generated through TCR intermediate (i.e. TCRint) cell differentiation in normal mice (i.e. via the extrathymic pathways and an alternative intrathymic pathway). It was investigated whether the generation of such clones in NTx mice follows this rule or whether they are generated by default via mainstream T cell differentiation in the thymus. The majority of T cells generated in NTx mice were TCRint cells in all organs tested. In contrast to athymic mice, which carry only TCRint cells with aging, a leaky appearance of high TCR (i.e. TCRhi) cells emerged in the lymph nodes and other organs of NTx mice. Self-reactive clones estimated by anti-Vbeta monoclonal antibodies in conjunction with the Mls system were confined to TCRint cells in all tested organs, including a target organ, the stomach, in NTx mice. A leaky population of TCRhi cells did not contain a significant number of self-reactive clones. Moreover, such self-reactive clones among TCRint cells in NTx mice with autoimmune disease were shown to be nonanergic in the proliferation assay. The present results suggest that the generation of self-reactive clones is totally due to TCRint cell differentiation, although it is still undetermined whether the expanding TCRint cell population is generated via the extrathymic pathway or an alternative intrathymic pathway. It is shown here not to be due to a failure of the TCRhi cell-differentiation pathway in NTx mice.

Animals↗
PubMed1996

Intraepithelial lymphocytes in colon have similar properties to intraepithelial lymphocytes in small intestine and hepatic intermediate TCR cells.

Recently, properties of intraepithelial lymphocytes (IEL) in the colon (C-IEL) have been analyzed in comparison with those of IEL in the small intestine (SI-IEL). We compared the properties of C-IEL with those of SI-IEL and hepatic intermediate TCR cells, two other types of extrathymic T cells. C-IEL and intermediate TCR cells contain many NK1+T cells, although SI-IEL contain few. V gamma and V delta usage of C-IEL was the same as that SI-IEL, and that of intermediate TCR cells was different. C-IEL responded to Con A while SI-IEL did not. As to adhesion molecules, C-IEL include both extrathymic and thymus-originated type T cells. With age, TCR- alpha beta(+) CD4+ CD8+ cells do not increase among C-IEL but do increase among SI-IEL. IL-2R beta(+) or CD4- CD8- C-IEL increase as observed in the liver. These results indicate that these organ-specific T cells have different roles at their respective sites and that they may be of different lineages.

Animals↗