The T lymphocyte glycoprotein CD2 binds the cell surface ligand LFA-3

Nature ◽  
1987 ◽  
Vol 326 (6111) ◽  
pp. 400-403 ◽  
Author(s):  
Periasamy Selvaraj ◽  
Marian L. Plunkett ◽  
Michael Dustin ◽  
Martin E. Sanders ◽  
Stephen Shaw ◽  
...  
Keyword(s):  
Cell Surface ◽  
T Lymphocyte ◽  
Surface Ligand

The murine homologue of the T lymphocyte CD2 antigen: molecular cloning, chromosome assignment and cell surface expression

1987 ◽  
Vol 17 (7) ◽  
pp. 1015-1020 ◽  
Author(s):  
William A. Sewell ◽  
Marion H. Brown ◽  
Michael J. Owen ◽  
Pamela J. Fink ◽  
Christine A. Kozak ◽  
...  
Keyword(s):  
Cell Surface ◽  
Molecular Cloning ◽  
T Lymphocyte ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Chromosome Assignment ◽  
Murine Homologue

Human Cytolytic T-Lymphocyte Clones and Their Function-Associated Cell Surface Molecules

1985 ◽  
pp. 559-573 ◽  
Author(s):  
Alan M. Krensky ◽  
Steven J. Mentzer ◽  
Julia L. Greenstein ◽  
Mary Crimmins ◽  
Carol Clayberger ◽  
...  
Keyword(s):  
Cell Surface ◽  
T Lymphocyte ◽  
Cell Surface Molecules ◽  
Surface Molecules ◽  
Cytolytic T Lymphocyte

scholarly journals A generic cell surface ligand system for studying cell-cell recognition

2019 ◽  
Author(s):  
Eleanor M Denham ◽  
Michael I Barton ◽  
Susannah M Black ◽  
Marcus J Bridge ◽  
Ben de Wet ◽  
...  
Keyword(s):  
Cell Surface ◽  
Surface Density ◽  
Cell Receptor ◽  
Surface Receptors ◽  
Ligand System ◽  
Ligand Interactions ◽  
A Cell ◽  
Surface Ligand ◽  
Receptor Biology ◽  
Cell Cell

AbstractDose-response experiments are a mainstay of receptor biology studies and can reveal valuable insights into receptor function. Such studies of receptors that bind cell surface ligands are currently limited by the difficulty in manipulating the surface density of ligands at a cell-cell interface. Here we describe a generic cell surface ligand system that allows precise manipulation of cell surface ligand densities over several orders of magnitude. We validate the system for a range of immunoreceptors, including the T cell receptor (TCR), and show that this generic ligand stimulates via the TCR at a similar surface density as its native ligand. This system allows the effect of surface density, valency, dimensions, and affinity of the ligand to be manipulated. It can be readily extended to other receptor-cell surface ligand interactions, and will facilitate investigation into the activation of, and signal integration between, cell surface receptors.

scholarly journals The terminology problem for T cells: a discussion paper

2000 ◽  
Vol 355 (1395) ◽  
pp. 361-362 ◽  
Author(s):  
Peter C. Doherty
Keyword(s):  
T Cells ◽  
Cell Surface ◽  
T Lymphocyte ◽  
Ludwig Wittgenstein ◽  
Cytotoxic T Lymphocyte ◽  
Cell Populations ◽  
Surface Markers ◽  
Cell Surface Markers ◽  
Discussion Paper ◽  
Thinking Processes

The school of thought that owes allegiance to Ludwig Wittgenstein teaches that language conditions perceptions. When we use the term ‘cytotoxic T lymphocyte’ or ‘helper Tcell’ we tend to orientate our own thinking processes, and those of listeners or readers, down particular paths. Part of the problem is that we are often describing cell populations by functions that may either be a property of only a proportion of those that are being assayed, or are simply inferred from the expression of various cell–surface markers. The consequence can be a measure of confusion that might be avoided if we could communicate with greater clarity. Is it possible to achieve a better terminology that will be accepted generally? The following are some examples of why there may be some value in thinking about this.

Gingipains Inactivate a Cell Surface Ligand onPorphyromonas gingivalisThat Induces TLR2- and TLR4-Independent Signaling

2006 ◽  
Vol 50 (4) ◽  
pp. 315-325 ◽  
Author(s):  
Mami Kishimoto ◽  
Atsutoshi Yoshimura ◽  
Mariko Naito ◽  
Kuniaki Okamoto ◽  
Kenji Yamamoto ◽  
...  
Keyword(s):  
Cell Surface ◽  
A Cell ◽  
Surface Ligand

scholarly journals A generic cell surface ligand system for studying cell–cell recognition

PLoS Biology ◽  
2019 ◽  
Vol 17 (12) ◽  
pp. e3000549 ◽  
Author(s):  
Eleanor M. Denham ◽  
Michael I. Barton ◽  
Susannah M. Black ◽  
Marcus J. Bridge ◽  
Ben de Wet ◽  
...  
Keyword(s):  
Cell Surface ◽  
Cell Recognition ◽  
Ligand System ◽  
Surface Ligand ◽  
Cell Cell

Alloreactive Cytolytic T Lymphocyte Precursor Cells in Aged C57B1 /6 nu/nu Mice: Frequency and Cell Surface Phenotype

2015 ◽  
pp. 21-24
Author(s):  
J. L. Maryanski ◽  
H. R. MacDonald ◽  
R. K. Lees ◽  
B. Sordat ◽  
J. -C. Cerottini
Keyword(s):  
Cell Surface ◽  
T Lymphocyte ◽  
Precursor Cells ◽  
Surface Phenotype ◽  
Cytolytic T Lymphocyte

Role of histocompatibility antigen gene and proto-oncogene expressions in intracerebral tumorigenicity of mouse neuroblastoma

1993 ◽  
Vol 78 (4) ◽  
pp. 619-629
Author(s):  
Toshiki Yamasaki ◽  
George Klein ◽  
Hans-Gustaf Ljunggren ◽  
Klas Kärre ◽  
Kouzo Moritake ◽  
...  
Keyword(s):  
Cell Surface ◽  
T Lymphocyte ◽  
Blot Analysis ◽  
Cytotoxic T Lymphocyte ◽  
Neuroblastoma Cell ◽  
Chain Gene ◽  
Transcriptional Level ◽  
Gene Expressions ◽  
Antigen Gene

✓ The role of N-myc, c-src, and major histocompatibility complex (MHC, H-2 in the mouse) class I antigen gene expressions in dimethyl sulfoxide (DMSO)-induced differentiation and intracerebral tumorigenicity was examined using a mouse MNB85 neuroblastoma cell line. A fluorescence-activated cell sorter disclosed cell-surface MHC enhancement by DMSO, causing an increase in cytotoxic T-lymphocyte sensitivity. Southern blot analysis verified a single copy of the proto-oncogenes and MHC deoxyribonucleic acids in both untreated and DMSO-treated MNB85 cells. Northern blot analysis indicated that DMSO treatment induced a decrease in N-myc and an increase in c-src and MHC messenger ribonucleic acids. Nuclear run-off transcription assay revealed down-regulation of N-myc at a posttranscriptional level, contrasted with primary up-regulation of c-src at a transcriptional level. Immunoprecipitation after treatment with enzyme endo-beta-N-acetyl-glycoseamidase H proved that the terminal glycosylation of MHC heavy-chain gene products normally occurs in the Golgi apparatus of MNB85 cells. Intracerebral tumorigenicity assay showed that cells highly MHC-expressed by DMSO were less tumorigenic than untreated cells in association with DMSO-augmented cytotoxic T-lymphocyte susceptibility. These results suggest that proto-oncogenes may be linked to cellular differentiation, while cell-surface MHC gene expression influences intracerebral immunosurveillance.

scholarly journals Rosetting of activated human T lymphocytes with autologous erythrocytes. Definition of the receptor and ligand molecules as CD2 and lymphocyte function-associated antigen 3 (LFA-3).

1987 ◽  
Vol 165 (3) ◽  
pp. 664-676 ◽  
Author(s):  
M L Plunkett ◽  
M E Sanders ◽  
P Selvaraj ◽  
M L Dustin ◽  
T A Springer
Keyword(s):  
Cell Adhesion ◽  
T Cell ◽  
T Lymphocytes ◽  
Cell Surface ◽  
T Lymphocyte ◽  
Surface Protein ◽  
Target Cells ◽  
Lymphocyte Function ◽  
Cell Surface Protein ◽  
Definition Of

CD2, also known as LFA-2, T11, and the E rosette receptor, is a T lymphocyte surface protein functionally important in adhesion to target cells and T cell triggering. LFA-3 is a widely distributed cell surface protein that functions in adhesion on target cells. We find that LFA-3 is expressed on human E, and that CD2 is a receptor for LFA-3 that mediates T cell adhesion to human E. Pretreatment of T lymphocytes with CD2 mAb or of E with LFA-3 mAb inhibits rosetting. Purified CD2 molecules bind to human E and inhibit rosetting. 125I-CD2 binding to E is inhibited by LFA-3 mAb; reciprocally, binding of LFA-3 mAb to human E is inhibited by pretreatment with purified CD2. Higher concentrations of CD2 aggregate human E; aggregation is inhibited by mAb to LFA-3.

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