B14-2-14 is a monoclonal cytotoxic IgM antibody which reacts with thymocytes of all mouse strains tested. The fraction of positive cells (by visual immunofluorescence) varies between strains from about 25-45% in A.CA to 65-85% in C57BL/6, and high levels are dominant in F1 hybrids. In the periphery, the antigen is found on a few percent of lymph node and not on splenic T cells, and it is absent in nude mice. Among thymocytes, the distribution of the B14 determinant largely overlaps with that of the TL antigen and of molecules binding peanut agglutinin. The B14 antibody reacts only minimally with hydrocortisone-resistant thymus cells. Biochemical analysis shows that B14 antibody, anti-TL antibody and peanut agglutinin bind to separate molecules. The target of the B14 antibody may be either an immature, thymic form of Thy-1, or another molecule associated with it. Two polypeptides, of 40 and 35 kDa are precipitated by both B14 and anti-Thy-1 antibodies from biosynthetically labeled thymus cell lysates, and two others, of 27 and 17 kDa, from surface-iodinated thymus cell preparations. B14-2-14 offers an additional method for identification and selection of thymocytes at different stages of differentiation, and should also be useful for studies of the Thy-1 antigen. 相似文献
A 20-year-old patient was hospitalized with clinical signs of acute appendicitis. After surgery, the histological findings in the appendix and a lymphatic node suggested the diagnosis of pseudoappendicitis caused by Plesiomonas shigelloides, which was isolated in pure culture from the lymphatic node. The strain of P. shigelloides was found to elaborate a heat-stable toxin and harbored two plasmids of 280 and 4 kilobases. A large plasmid has previously been implicated as a virulence marker in P. shigelloides infections. 相似文献
Summary A large number of human haematopoietic cell lines was examined for spontaneous production of interferon. Unconcentrated culture supernatants from 70 out of 71 B-lymphoblastoid cell lines contained considerable amounts of interferon (median titer 22 units per ml); a few lines produced more than 100 units/ml with peak values up to 500 units/ml. In contrast, only one B-lymphoma line out of 18 genuine lymphoma, myeloma, and leukaemia cell lines tested spontaneously produced small amounts of interferon. Following treatment with 5-bromodeoxyuridine (BrdUrd), interferon was produced without further induction in most B-lymphoid cell lines, but not in any of the non-B, non-T, T-lymphoid or myeloid lines examined.Modulation of spontaneous interferon production by chemicals (sodium butyrate, dexamethasone, dimethylsulfoxide, a phorbol ester, and BrdUrd) was studied in more detail in three B-lymphoblastoid and four B-lymphoma cell lines. The patterns of responses observed were different for the action of different chemicals on a given cell line as well as between lymphoblastoid and lymphoma lines in general; furthermore, several lines of evidence suggest that chemicals can differentially influence spontaneous and virus-induced interferon production in a given cell line.The composition of spontaneously produced interferon was analysed using antisera specific for HuIFN- and HuIFN-. Interferons produced by untreated as well as BrdUrd-treated lymphoblastoid cells contained more than 95 per cent IFN-, whereas BrdUrd-treated lymphoma cells produced IFN- as well as minor amounts (cell lines Namalwa and NC-37) or even over 90 per cent of IFN- (Daudi).With 2 Figures 相似文献
An immunohistochemical and morphometric analysis was performed on trephine biopsy specimens of the bone marrow in 40 patients (23 men and 17 women, mean age 62 years) with different subtypes of myelodysplastic syndromes (MDS) to determine dysmegakaryopoiesis, but particularly precursor cells--that is, pro- and megakaryoblasts. In 31 of the 40 patients the numbers of megakaryocytes were increased which was associated with a predominance of smaller cell forms (micromegakaryocytes). Compared with periodic acid Schiff, immunostaining with a formalin resistant monoclonal antibody against glycoprotein IIIa (Y2/51(CD61) showed a clinically important proportion of immature elements. These could be designated pro- and megakaryoblasts by taking morphometric measurements on smears and bone marrow sections. There was a relevant increase in the number of promegakaryoblasts in 32 patients, consistent with uncontrolled expansion of the precursor pool. Seventeen repeated bone marrow biopsy specimens taken after chemotherapy largely showed a decrease in the numbers of megakaryocytes including the precursor cell population. Moreover, morphometric evaluation disclosed that micromegakaryocytes in MDS differ significantly from those in chronic myeloid leukaemia (CML) due to distinctive nuclear features and a disturbed nuclear:cytoplasmic ratio. These changes generate a more pleomorphic or atypical appearance of this cell population in MDS, compared with micromegakaryocytes in CML. It is concluded that the disproportionate increase in megakaryocyte precursors and the grossly abnormal aspects of micromegakaryocytes in MDS are characteristics of the severe defect involving haematopoiesis in this disorder. 相似文献
The common γ chain (γc) forms a critical component of the receptors for interleukins (IL)-2, IL-4, IL-7, IL-9, and IL-15. We analyzed γc-deficient mice to define a role for γc signaling in the development and function of the macrophage lineage. No major differences in absolute cell numbers, cell surface phenotype, or in vitro function of γ?c compared to γ+c macrophages were observed. We therefore conclude that signaling through the γc chain is not essential for the differentiation of mouse macrophages. Although B and T cells require γc for IL-4 responses, IL-4 up-regulated major histocompatibility class II molecules and inhibited nitric oxide production from γ?c macrophages following stimulation with lipopolysaccharide and interferon-γ. γ?c macrophages could also respond to IL-13, consistent with the model of a type II IL-4 receptor α/IL-13R which can function in the absence of γc. Both IL-4 and IL-13 responses could be completely inhibited with the mouse IL-4 antagonist QY, suggesting that all of the observed IL-13 responses pass through the type II receptor, making it the primary signaling receptor complex for IL-13 in mouse macrophages. 相似文献
Relationships between CD45 and p56Ick have been suggested by co-immunoprecipitation of both proteins and by dephosphorylation of the p56lck regulatory site, Tyr 505, by CD45 in vitro. We investigated whether the kinase activity of p56lck is modulated in T cells triggered via CD45. We showed that incubation of Jurkat cells with a combination of two anti-CD45 monoclonal antibodies (mAb) (MC5/2 + D3/9) induced an increase in p56lck kinase activity, while a single mAb did not. Under these conditions, p56lck underwent two consecutive waves of activation. This was accompanied by internalization of the kinase and by a time-dependent increased accessibility of CD45 phosphatase at the plasma membrane. Similarly, activation and internalization of p56lck were observed using a combination of anti-CD45 (MC5/2) and anti-CD2(T112) mAb, suggesting that a functional complex consisting of CD45, CD2 and p56lck was formed upon cell triggering. Taken together, these results suggests that: (i) CD45 participates in the regulation of p56lck kinase activity in vivo and that (ii) CD45 could play a mediator role in the stimulation and endocytosis of p56lck through the CD2 pathway. 相似文献
To investigate whether histamine receptor ligands influence thein vivo-release of acetylcholine in the ventral striatum, this brain region was superfused with histamine receptor agonists or antagonists through a push-pull cannula and drug effects on the release of acetylcholine were investigated.
Histamine, the H1 receptor agonist 2-thiazolyl-ethylamine and the H3 receptor antagonist thioperamide enhanced acetylcholine release, while the H3 receptor agonist (R)-α-methylhistamine was ineffective. The results indicate that H1 receptors and H3 receptors modulate acetylcholine release.
The thioperamide-induced increase of acetylcholine release might be exerted via H3-receptors located on cholinergic terminals. Alternatively, thioperamide might enhance acetylcholine release by incresing endogenous histamine release via H3 autoreceptors.
It is concluded that, via stimulation of striatal H1- and H3 receptors, histaminergic neurons are involved in the regulation of cholinergic neuronal activity in the ventral striatum.