scholarly journals A New Marker on Chicken Hematopoietic Cells is Defined by a Monoclonal Antibody Raised Against a VßChain of the Human TCR

1992 ◽  
Vol 2 (4) ◽  
pp. 273-284
Author(s):  
Anne-Sophie Lacoste-Eleaume ◽  
Christian Bleux ◽  
Catherine Corbel ◽  
Dominique Carriere ◽  
Philippe Poncelet ◽  
...  

In this paper, we show that a mouse monoclonal antibody, 111-427, specific for the Vß5.3 chain of the human T-cell receptor (TCR) for antigen, also reacts with chicken hematopoietic cells. Our data indicate that the majority of 111-427 positive cells among peripheral blood leucocytes (PBL) are thrombocytes. This antibody also recognizes two in vitro cell lines, III-C5, an IL-2-dependent T-cell-line and HD11, a macrophage cell line. In addition, erythrocytes and a minor subpopulation of thymus and spleen cells are also stained by the monoclonal antibody (mAb). No specific immunoprecipitation could be detected from125I radiolabeled cell lysates. By Western blotting techniques, the 111- 427 mAb identifies a single band of apparent molecular weight 91 kD, unaffected by reduction, from III-C5 and HD11 cell lysates. This band is absent in negative cell control lysates. On thrombocytes, the apparent molecular weight of the band is shifted to 87 kD. These results indicate that the mAb does not recognize the chicken T-cell receptor for antigen, but a cell surface marker shared primarily between thrombocytes and erythrocytes. This new chicken cell marker is compared to other cell surface markers in avian or mammalian species that present some analogies in their tissue distribution.

Blood ◽  
2008 ◽  
Vol 112 (13) ◽  
pp. 5103-5110 ◽  
Author(s):  
Jennifer M. L. Tjon ◽  
Wieke H. M. Verbeek ◽  
Yvonne M. C. Kooy-Winkelaar ◽  
Binh H. Nguyen ◽  
Arno R. van der Slik ◽  
...  

Abstract Enteropathy-associated T-cell lymphoma, an often fatal complication of celiac disease, can result from expansion of aberrant intraepithelial lymphocytes in refractory celiac disease type II (RCD II). Aberrant intraepithelial lymphocytes and lymphoma cells are intracellularly CD3ϵ+ but lack expression of the T-cell receptor (TCR)–CD3 complex on the cell surface. It is unknown what causes the loss of TCR-CD3 expression. We report the isolation of a cell line from an RCD II patient with the characteristic phenotype of enteropathy-associated T-cell lymphoma. We demonstrate that in this cell line the TCR-α and -β chains as well as the CD3γ, CD3δ, CD3ϵ, and ζ-chains are present intracellularly and that assembly of the CD3γϵ, CD3δϵ, and ζζ-dimers is normal. However, dimerization of the TCR chains and proper assembly of the TCR-CD3 complex are defective. On introduction of exogenous TCR-β chains, but not of TCR-α chains, assembly and functional cell surface expression of the TCR-CD3 complex were restored. Defective synthesis of both TCR chains was found to underlie loss of TCR expression in similar cell lines isolated from 2 additional patients. (Pre)malignant transformation in RCD II thus correlates with defective synthesis or defective association of the TCR chains, resulting in loss of surface TCR-CD3 expression.


1987 ◽  
Vol 165 (4) ◽  
pp. 1141-1159 ◽  
Author(s):  
M S Krangel

An assay has been developed to assess the dynamics of cell surface glycoproteins, in which neuraminidase digestion of intact cells is used to determine the fate of cell surface molecules initially labelled via lactoperoxidase-catalyzed iodination. This approach has been used to demonstrate the constitutive endocytosis and recycling of the T3-T cell receptor (T CR) complex on the human T leukemic cell line HPB-MLT. Stable populations of both phosphorylated and nonphosphorylated forms of the T3 gamma peptide have been identified in these cells. Whereas the former are constitutively endocytosed, the latter appear to be excluded from this pathway. The results presented indicate that T3 gamma phosphorylation may control the endocytosis and recycling of the T3-TCR complex on this cell line.


1991 ◽  
Vol 174 (4) ◽  
pp. 891-900 ◽  
Author(s):  
S M Friedman ◽  
M K Crow ◽  
J R Tumang ◽  
M Tumang ◽  
Y Q Xu ◽  
...  

While all known microbial superantigens are mitogenic for human peripheral blood lymphocytes (PBL), the functional response induced by Mycoplasma arthritidis-derived superantigen (MAM) is unique in that MAM stimulation of PBL consistently results in T cell-dependent B cell activation characterized by polyclonal IgM and IgG production. These immunostimulatory effects of MAM on the humoral arm of the human immune system warranted a more precise characterization of MAM-reactive human T cells. Using an uncloned MAM reactive human T cell line as immunogen, we have generated a monoclonal antibody (mAb) (termed C1) specific for the T cell receptor V beta gene expressed by the major fraction of MAM-reactive human T cells, V beta 17. In addition, a V beta 17- MAM-reactive T cell population exists, assessed by MAM, induced T cell proliferation and cytotoxic T cell activity. mAb C1 will be useful in characterizing the functional properties of V beta 17+ T cells and their potential role in autoimmune disease.


1989 ◽  
Vol 30 (3) ◽  
pp. 162-168 ◽  
Author(s):  
Maria Lipoldova ◽  
Arthur W. Boylston ◽  
Hans Yssel ◽  
Michael J. Owen

1992 ◽  
Vol 175 (4) ◽  
pp. 907-915 ◽  
Author(s):  
S Yoshino ◽  
L G Cleland

The effects of treatment with a monoclonal antibody (R73 mAb) against T cell receptor alpha/beta (TCR-alpha/beta) on both established adjuvant arthritis (EAA) and established collagen-induced arthritis (ECIA) in rats have been investigated. Rats were treated with R73 mAb when arthritis reached a peak. Treatment with the anti-TCR-alpha/beta mAb markedly suppressed EAA, whereas ECIA was not affected by the mAb treatment. Histologically, R73 mAb-treated rats with EAA showed mild hyperplasia of synovial tissues, sparse infiltration of inflammatory cells, and minimal erosion of cartilage, whereas arthritic rats treated with PBS and an irrelevant control mAb against Giardia had marked hyperplasia of synovium with pannus, massive inflammatory cell infiltrate, and severe destruction of cartilage and subchondral bone. R73 mAb-treated rats with ECIA exhibited pronounced formation of pannus containing many inflammatory cells and marked cartilage and subchondral damage similar to those in arthritic rats that received the control treatments. Treatment with R73 mAb depleted markedly alpha/beta+ T cells in both peripheral blood and synovial tissues of rats with EAA and ECIA. R73 mAb treatment was associated with marked reduction in arthritogen-specific delayed-type hypersensitivity responses in both EAA and ECIA. The titers of antibodies against type II collagen produced in rats with ECIA were not affected by the mAb. Thus, alpha/beta+ T cells appear to have a central role in EAA, but not in chronic ECIA.


Oncotarget ◽  
2018 ◽  
Vol 9 (75) ◽  
pp. 34132-34141 ◽  
Author(s):  
Soyoko Morimoto ◽  
Fumihiro Fujiki ◽  
Kenta Kondo ◽  
Hiroko Nakajima ◽  
Yoshiki Kobayashi ◽  
...  

FEBS Letters ◽  
2003 ◽  
Vol 546 (2-3) ◽  
pp. 379-384 ◽  
Author(s):  
Min Kyung Kim ◽  
Yoon-La Choi ◽  
Min Kyung Kim ◽  
Seok-Hyung Kim ◽  
Eun Young Choi ◽  
...  

2007 ◽  
Vol 120 (15) ◽  
pp. 1319-1325 ◽  
Author(s):  
Zhao-hui WANG ◽  
Yu-hua LIAO ◽  
Jing YUAN ◽  
Li ZHANG ◽  
Min WANG ◽  
...  

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