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Biomedical subjects

R Abe

Publications and source records attributed to R Abe.

At least 433 records · Page 24Linked to original sources

Regulation of allotype-linked NPb idiotype by an idiotype-positive soluble factor derived from a T cell hybridoma. Coupling of the circuit regulation to the network concept.

We reported in this paper genetic requirements for the suppression of anti-4-hydroxy-3-nitrophenylacetyl (NP) antibody response induced by an NP-specific, Igh-1 linked idiotype (NPb) positive T suppressor factor (NPb-TsF) derived from a T cell hybridoma 7C3-13 of B10.BR (Igh-1b, H-2k) mouse origin. NPb-TsF could suppress the responses mounted by primed spleen cells of all IgVH compatible strains regardless of their H-2 haplotypes. The majority of the anti-NP antibody response suppressed by NPb-TsF was idiotype positive (Id+). NPb-TsF was also capable of suppressing the responses of H-2 compatible but Igh incompatible strains where responding cells do not produce NPb idiotype. NPb-TsF was incapable of suppressing the responses of mouse strains who are incompatible both in IgVH and H-2 loci, indicating that the identity in either IgVH or H-2 genes between NPb-TsF and responding cells was necessary for the initiation of the suppression by NPb-TsF. It was further found that the NPb-TsF utilizes anti-idiotypic Lyt-1+2+3+ T cells (transducer cells), which are present only in IgVH compatible strains, to ultimately suppress the Id+ antibody production by B cells. These results indicate that there exists a pathway where an idiotypic NPb-TsF activates a suppressor circuit mediated via the idiotype-antiidiotype interactions apart from the previously described carrier-specific and H-2 restricted suppressor circuit. Both pathways involve the 'transduction' step utilizing Lyt-1+2+3+ intermediary T cells. Our experiments provide important clues for coupling the two major immunological concepts, network and circuit.

Animals↗

Lectin-binding patterns of breast carcinoma: significance on structural atypism.

We have investigated lectin-binding profiles of the human breast epithelia and the structural atypism in intraductal carcinoma. The lectino-histochemical probes using biotin-labeled peanut agglutinin (PNA), soybean agglutinin (SBA) and wheat germ agglutinin (WGA) with avidin-biotin peroxidase complex were performed on formalin-fixed and paraffin-embedded specimens from 24 patients. While normal and benign hyperplastic epithelia were stained almost in luminal borders and apical cytoplasmic surfaces, intraductal carcinoma additionally showed conspicuous staining of intracytoplasmic lumina and supranuclear cytoplasmic margins. The lectin-binding pattern found in papillary hyperplasia was completely different from that in intraductal carcinoma; the former was an irregular network structure along luminal borders, whereas the latter was not only a cribriform but also a rosette structure along intracytoplasmic lumina and supranuclear cytoplasms. Such lectin-binding patterns seemed to reflect the change of cell polarity in malignant transformation. The significance of these observations in elucidation of structural atypism was discussed in relation to 3-D structure of intraductal carcinoma.

Biotin↗

Is there multiplicity in I-J subregion products?

Recent studies in molecular genetics have revealed the striking fact that the previously known I-J subregion (or I-J gene) does not exist at the exactly prescribed position in the I-region of the murine major histocompatibility complex (MHC). How, then, can we comprehend the established serological and functional significance of I-J genes and I-J products? To answer this question we reexamined systematically the specificities and functional activities of monoclonal anti-I-J antibodies. A series of monoclonal anti-I-Jk antibodies were newly established by fusion of B10.A(3R) spleen cells immune to B10.A(5R) lymphoid cells with P3X63-Ag8-653. Their abilities to eliminate known functions of T cell subsets and to react with I-J+ T cell clones of defined functions were examined in an in vitro secondary antibody response and by fluorescence-activated cell sorter analysis. The monoclonal antibodies (mAb) were divided into three groups: (1) those reactive with suppressor inducer T cells (Tsi), Tsi hybridomas, and the antigen-specific T cell factor (TsF) derived from them; (2) those specific for suppressor effector T cells (Tse) and Tse clones; and (3) those reactive with some but not all helper T cells. The determinants detected by these three different groups of antibodies are apparently present on separate, nonoverlapping cell populations and functionally distinct clones. The above results indicate the multiplicity of I-J products expressed on different T cell subsets, and sharply contradict the notion, derived from molecular genetics, that not even a single gene can be accommodated in the I-J subregion. To resolve this dilemma, we compared the above results with those obtained with another set of mAb that also detected I-region-controlled determinants on augmenting and helper T cells. Although the specificities of these mAb clearly mapped to within the I-region, none of them reacted with conventional class II Ia antigens of B cells and macrophages. The common properties shared by these anti-Ik and anti-I-Jk antibodies are that (1) they react only with T cells and T cell clones with I-region-controlled functions; (2) they can block some of the Ia-restricted cell interactions, including those of helper and suppressor T cells; and (3) they inhibit the syngeneic and/or allogeneic mixed lymphocyte reaction (MLR) by blocking the responder but not the stimulator cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

[Prevention of 5-FU induced toxicity in C3 H/HE mice with interferon or with interferon inducers (poly 1: C, OK-432, Lentinan)].

It is well known that all cell lines, normal as well as malignant, have a sensitivity to the growth-inhibitory effect of Interferon, or Interferon inducers. 5-FU is a widely used anticancer drug considered to be a cell cycle-specific agent. We speculated that the antiproliferative effect of Interferon or Interferon inducers might affect the activity of 5-FU and diminish the uncomfortable side-effects of this agent. Initially this experiment, we observed the mortality rate in mice after administration of 5-FU alone, or 5-FU plus Interferon (alpha inducers). We then carried out cytofluorometric observation of bone marrow cells, and finally studied the influence of Interferon (or inducers) on the anticancer effects of 5-FU against MM48 tumors in C3/He mice. Findings were as follow: 1) Administration of beta-type Interferon for 2 days, following the administration of a toxic dose (140 mg/kg/w) of 5-FU, revealed significant protection from mortality in C3H/He mice. This effect was also observed when Interferon inducers (Poly I: C, OK-432, Lentinan) were administered with 5-FU. Body weight loss was 10.4% at nadir in mice treated with 5-FU alone, while there was a body weight gain of 36.3% in mice treated with 5-FU plus Interferon. 2) Cytofluorometry of bone marrow cells obtained from mice femur at timed intervals after the administration of OK-432, or Lentinan indicated that these drugs inhibited the entry of cells into the S-phase, causing then to accumulated in the G0.G1-phase during the first 48 hours. 3) Histological findings of intestinal mucosa in mice showed prominent destruction after bolus injection of 350 mg/kg of 5-FU alone, while these findings were not observed in mice after the bolus injection of 350 mg/kg of 5-FU combined with Interferon. 4) The tumor volume ratio (T/C) was significantly reduced in the group treated with 5-FU alone as well as that treated with 5-FU combined with Interferon (or inducers) in C3H/He mice bearing MM48 tumors. All mice were dead about 2 weeks after administration of 5-FU alone, while all mice treated with 5-FU plus Interferon (or inducers) were alive in the same period. From these results, we speculate that Interferon, or Interferon inducers play an important role in the prevention of side effects of cell cycle-specific cytotoxic drugs like 5-FU, without decreasing their anticancer activity.

Animals↗

[Lipid-secreting carcinoma of the breast].

Lipid secreting carcinoma is a very rare tumor of the breast. This is regarded as a special type of breast carcinoma, which is characterized by abundant intracytoplasmic neutral lipid stained with Sudan IV. Two cases (75 and 42 year old females) of lipid secreting carcinoma of the breast are presented. No other reports of lipid secreting carcinoma have been available in the Japanese literature. In this report, the physical, mammographic and ultrasonographic diagnosis and pathological findings are described and discussed.

Adult↗

[Susceptibility of intraductal papillomas to carcinogenesis based on 3-dimensional reconstruction study].

Surgical specimens from 16 patients with intraductal papilloma were subjected to 3-dimensional reconstruction studies of mammary ducts in order to detect early cancerous foci developing in papilloma, to analyze growth behavior of papilloma and to establish morphological features of papilloma particularly prone to cancerous change. Papilloma of the multiple type (10 cases) originated in the terminal duct lobular units (TDLU), while papilloma of the solitary type (6 cases) originated in the large ducts except for one. In 4 out of the 16 patients small foci of intraductal carcinoma were found during specimen reconstruction. Two of the four patients harbored minimal cancer as small as 3 mm or less. The carcinomas with multifocal origins in the TDLUs were anatomically connected with peripheral papilloma so far as to take the form of "cancer in papilloma". Papilloma preceding carcinoma was of the multiple type in 3 cases and of the solitary type in one. But according to the sites from which papillomas originated, 4 out of the 11 cases originating in the TDLU had cancerous foci, whereas none of the 5 cases originating in the large ducts did. This suggests that the peripheral papilloma is highly susceptible to cancerous change. From a clinical point of view, we proposed a nomenclature of peripheral vs. central papillomas instead of the conventional multiple vs. solitary.

Breast Neoplasms↗

Monoclonal suppressor factor specific for lactate dehydrogenase B. I. Mechanism of interaction between the factor and its target cells.

Hybridomas secreting a monoclonal T suppressor-effector factor (TseF) were produced by fusion of a lactate dehydrogenase B (LDHB)-specific long-term T suppressor-effector (Tse) cell line with the BW5147 thymoma. A short exposure (4 h) to TseF completely suppresses the antigen-specific and A-restricted proliferation of LDHB-primed Lyt-1+2- [possibly helper (Th)] cells. The action of TseF on Th cells, as that of the Tse cells themselves, is antigen-specific and A-restricted. The interaction of TseF with Th cells involves two binding events, of which one occurs via antigen bridge, and the other represents the recognition of a factor-derived Ak-like moiety by the anti-Ak receptor of Th cells. The Ak-like moiety of the TseF carries the determinants that serve as restriction elements for antigen recognition by Th cells, and additional determinants demonstrable by T cell-specific monoclonal "anti-Ak" antibodies, however, it lacks serologically detectable determinants of the B cell-derived A alpha A beta class II Mhc molecules.

Animals↗

Cytogenetic findings in congenital leukemia: case report and review of the literature.

The cytogenetic findings in a five-week-old female infant with acute lymphoblastic leukemia (ALL) are reported. Markers 11q - and 19 + were observed and considered to be due to an interstitial deletion of segment 11q13 to 11q23 of chromosome #11 and an insertion of this segment into the terminal region of the short arm of #19. Previously published banded cases of leukemic infants under one year of age have been summarized. A review of the data in these 29 cases suggests that the appearance of a normal karyotype in acute leukemia of infants (less than or equal to 1 year old) is much less common than in other categories of acute leukemia. Fourteen out of 29 cases (48%) had chromosomal abnormalities involving 11q. Seven of eight ALL cases had aberrations with a breakpoint at 11q22-23; six cases had t(4;11), one case had a del(11q) and ins(19p), and another had a t(1;22;4). All of three AMMoL cases had translocations involving the long arm of #11. The percentage of patients with t(4;11) and certain translocations involving 11q in infants with ALL or AMMoL, respectively, is higher than that seen in ALL and AMMoL in general. Eleven out of 12 cases (92%) of infant acute leukemias with chromosomal abnormalities involving 11q22-23 were five months old or less.

Chromosome Deletion↗

Kappa and lambda immunoglobulin expression associated with abnormalities of chromosomes #2 and #22 in lymphoma and leukemia.

The types of surface immunoglobulins on Burkitt lymphoma (BL) cells correlate with the specific chromosomes that are altered in the tumor. For example, BL with a t(2;8) translocation expresses kappa (kappa) light chains, whereas BL with a t(8;22) translocation expresses lambda (lambda) light immunoglobulin chains; these correspond with the locations of the kappa chain genes on chromosome #2 and the lambda chain genes on chromosome #22, respectively (1-5). In order to explain this close correlation between specific translocations and light chain expression in BL and BL-type acute lymphocytic leukemia (ALL) (L3 type), Hecht et al. [6] proposed the concept of position effect, which is reviewed herein.

Adolescent↗