Monoclonal antibody against a conjugation-specific nuclear antigen in Paramecium caudatum

1990 ◽  
Vol 95 (2) ◽  
pp. 287-291
Author(s):  
AKIRA YANAGI ◽  
HIROAKI YAMAMOTO

To understand molecular mechanisms controlling the sexual reproduction process (conjugation) in Paramecium caudatum, we have tried to detect conjugation-specific antigens with monoclonal antibodies. We obtained a monoclonal antibody (CSN-1) against an antigen that appears in the nuclei only during conjugation. This nuclear antigen began to appear both in micro- and macronuclei at micronuclear stage II or III early in the conjugation process (4 h after the mating reaction at 25°C). In the macronucleus, the nuclear antigen persisted until the stage of macronuclear fragmentation (about 35 h) and then disappeared before degeneration of the macronuclear fragments. In the micronucleus, the antigen existed until the crescent stage (stage V) of the first meiotic division (8h). The antigen in the micronucleus disappeared after the crescent stage but reappeared again in the eight nuclei produced by the third postzygotic division (25 h). Then it persisted only in the four macronuclear anlagen differentiated from the eight nuclei (about 30 h). When exconjugant cells had undergone two successive postconjugational cell divisions and thus possessed only one new macronucleus as in the vegetative cells, the antigen disappeared completely from the new macronucleus in most cells. These cells without the antigen began to appear about 50 h after the mating reaction. As the antigen is specific to conjugation and localized in nuclei, it may play some important role(s) in the conjugation process.

1990 ◽  
Vol 46 (1) ◽  
pp. 50-55 ◽  
Author(s):  
Jasper J. Quak ◽  
Guus Van Dongen ◽  
Marie A. E. Koken ◽  
Joost G. P. Brakkee ◽  
Rik J. Scheper ◽  
...  

2013 ◽  
Vol 34 (6) ◽  
pp. 619-624 ◽  
Author(s):  
Antonino Catanzaro ◽  
Charles Daley

Studies over the past several decades have dramatically increased our understanding of the immune response to Mycobacterium tuberculosis infection, and advances in proteomics and genomics have led to a new class of immune-diagnostic tests, termed interferon-γ (IFN-γ) release assays (IGRAs), which appear to obviate many of the problems encountered with the tuberculin skin test (TST). Worldwide, 2 IGRAs are currently commercially available. QuantiFERON-TB Gold In-Tube (Cellestis) is a third-generation product that uses an enzyme-linked immunosorbent assay to measure IFN-γ generated in whole blood stimulated with M. tuberculosis–specific antigens. T-Spot-TB (Oxford Immunotec) employs enzyme-linked immunosorbent spot technology to enumerate the number of purified lymphocytes that respond to M. tuberculosis–specific antigens by producing IFN-γ. These in vitro tests measure the host immune response to M. tuberculosis–specific antigens, which virtually eliminates false-positive cross reactions caused by bacillus Calmette-Guérin vaccination and/or exposure to environmental nontuberculous mycobacteria that plague the interpretation and accuracy of the tuberculin skin test (TST). The high specificity of IGRAs, together with sensitivity commensurate with or better than that of the TST, promises an accurate diagnosis and the ability to focus tuberculosis-control activities on those who are actually infected with M. tuberculosis. The Third Global Symposium was held over a 3-day period and was presented by the University of California, San Diego, Continuing Medical Education department; slides and sound recordings of each presentation are available at http://cme.ucsd.edu/igras/syllabus.html. A moderated discussion is also available at http://cme.ucsd.edu/igrasvideo. This document provides a summary of the key findings of the meeting, specifically focusing on the use of IGRAs in screening healthcare worker populations.


1987 ◽  
Vol 105 (2) ◽  
pp. 983-990 ◽  
Author(s):  
S Jalkanen ◽  
R F Bargatze ◽  
J de los Toyos ◽  
E C Butcher

The tissue-specific homing of lymphocytes is directed by specialized high endothelial venules (HEV). At least three functionally independent lymphocyte/HEV recognition systems exist, controlling the extravasation of circulating lymphocytes into peripheral lymph nodes, mucosal lymphoid tissues (Peyer's patches or appendix), and the synovium of inflamed joints. We report here that antibodies capable of inhibiting human lymphocyte binding to one or more HEV types recognize a common 85-95-kD lymphocyte surface glycoprotein antigen, defined by the non-blocking monoclonal antibody, Hermes-1. We demonstrate that MEL-14, a monoclonal antibody against putative lymph node "homing receptors" in the mouse, functionally inhibits human lymphocyte binding to lymph node HEV but not to mucosal or synovial HEV, and cross-reacts with the 85-95-kD Hermes-1 antigen. Furthermore, we show that Hermes-3, a novel antibody produced by immunization with Hermes-1 antigen isolated from a mucosal HEV-specific cell line, selectively blocks lymphocyte binding to mucosal HEV. Such tissue specificity of inhibition suggests that MEL-14 and Hermes-3 block the function of specific lymphocyte recognition elements for lymph node and mucosal HEV, respectively. Recognition of synovial HEV also involves the 85-95-kD Hermes-1 antigen, in that a polyclonal antiserum produced against the isolated antigen blocks all three classes of lymphocyte-HEV interaction. From these studies, it is likely that the Hermes-1-defined 85-95-kD glycoprotein class either comprises a family of related but functionally independent receptors for HEV, or associates both physically and functionally with such receptors. The findings imply that related molecular mechanisms are involved in several functionally independent cell-cell recognition events that direct lymphocyte traffic.


1985 ◽  
Vol 33 (9) ◽  
pp. 951-953 ◽  
Author(s):  
J A Simson ◽  
R Dom ◽  
J Chao ◽  
C Woodley ◽  
L Chao ◽  
...  

A specific monoclonal antibody against rat tissue kallikrein was used as the primary antibody for indirect immunoperoxidase staining of rat hypothalamus. Kallikrein was localized in the epithelial cells (ependyma) lining the third ventricle as well as in cell bodies of arcuate, supraoptic, paraventricular, and ventromedial nuclei.


Polymers ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1422 ◽  
Author(s):  
Marcinkowska ◽  
Stanczyk ◽  
Janaszewska ◽  
Gajek ◽  
Ksiezak ◽  
...  

Taxanes are considered fundamental drugs in the treatment of breast cancer, but despite the similarities, docetaxel (doc) and paclitaxel (ptx) work differently. For this reason, it is interesting to identify mechanisms of antitumor activity of PAMAM dendrimer conjugates that carry docetaxel or paclitaxel and monoclonal antibody trastuzumab, specifically targeted to cells which overexpressed HER-2. For this purpose, the impact on the level of reactive oxygen species, the mitochondrial membrane potential, cell cycle distribution and the activity of caspases-3/7, -8 and -9 of PAMAM-doc-trastuzumab and PAMAM-ptx-trastuzumab conjugates was determined and compared with free docetaxel and paclitaxel toward HER-2-positive (SKBR-3) and negative (MCF-7) human breast cancer cell lines. Moreover, apoptosis and necrosis were studied using flow cytometry and confocal microscopy, respectively. Our studies show the complexity of the potential mechanism of cytotoxic action of PAMAM-drug-trastuzumab conjugates that should be sought as a resultant of oxidative stress, mitochondrial activation of the caspase cascade and the HER-2 receptor blockade.


Biomedicines ◽  
2020 ◽  
Vol 8 (11) ◽  
pp. 507
Author(s):  
Andras Franko ◽  
Lucia Berti ◽  
Jörg Hennenlotter ◽  
Steffen Rausch ◽  
Marcus O. Scharpf ◽  
...  

Type 2 diabetes (T2D) is associated with worse prognosis of prostate cancer (PCa). The molecular mechanisms behind this association are still not fully understood. The aim of this study was to identify key factors, which contribute to the more aggressive PCa phenotype in patients with concurrent T2D. Therefore, we investigated benign and PCa tissue of PCa patients with and without diabetes using real time qPCR. Compared to patients without diabetes, patients with T2D showed a decreased E-cadherin/N-cadherin (CDH1/CDH2) ratio in prostate tissue, indicating a switch of epithelial-mesenchymal transition (EMT), which is a pivotal process in carcinogenesis. In addition, the gene expression levels of matrix metalloproteinases (MMPs) and CC chemokine ligands (CCLs) were higher in prostate samples of T2D patients. Next, prostate adenocarcinoma PC3 cells were treated with increasing glucose concentrations to replicate hyperglycemia in vitro. In these cells, high glucose induced expressions of MMPs and CCLs, which showed significant positive associations with the proliferation marker proliferating cell nuclear antigen (PCNA). These results indicate that in prostate tissue of men with T2D, hyperglycemia may induce EMT, increase MMP and CCL gene expressions, which in turn activate invasion and inflammatory processes accelerating the progression of PCa.


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