Non-specific influx of T-cell receptor alpha/beta and gamma/delta lymphocytes in mucosal biopsies from a patient with orofacial granulomatosis

2000 ◽  
Vol 29 (10) ◽  
pp. 519-522 ◽  
Author(s):  
F. Facchetti ◽  
S. Signorini ◽  
A. Majorana ◽  
M. A. Manganoni ◽  
P. Sapelli ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Gamma Delta ◽  
Receptor Alpha ◽  
Orofacial Granulomatosis ◽  
Alpha Beta ◽  
Cell Receptor Alpha

Lymphoid development in mice congenitally lacking T cell receptor alpha beta-expressing cells

Science ◽  
1992 ◽  
Vol 256 (5062) ◽  
pp. 1448-1452 ◽  
Author(s):  
K. Philpott ◽  
J. Viney ◽  
G Kay ◽  
S Rastan ◽  
E. Gardiner ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Lymphoid Development ◽  
Receptor Alpha ◽  
Alpha Beta ◽  
Cell Receptor Alpha

scholarly journals The presumptive CDR3 regions of both T cell receptor alpha and beta chains determine T cell specificity for myoglobin peptides.

1990 ◽  
Vol 172 (1) ◽  
pp. 27-33 ◽  
Author(s):  
J S Danska ◽  
A M Livingstone ◽  
V Paragas ◽  
T Ishihara ◽  
C G Fathman
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Amino Acid Sequences ◽  
Antigenic Specificity ◽  
Antigenic Peptides ◽  
Surface Complexes ◽  
Receptor Alpha ◽  
Alpha Beta ◽  
Cell Receptor Alpha

The T cell receptor alpha/beta (TCR-alpha/beta) is encoded by variable (V), diversity (D), joining (J), and constant (C) segments assembled by recombination during thymocyte maturation to produce a heterodimer that imparts antigenic specificity to the T cell. Unlike immunoglobulins (Igs), which bind free antigen, the ligands of TCR-alpha/beta are cell surface complexes of intracellularly degraded antigens (i.e., peptides) bound to and presented by polymorphic products of the major histocompatibility complex (MHC). Therefore, antigen recognition by T cells is defined as MHC restricted. A model has been formulated based upon the similarity between TCR-alpha/beta V region and Ig Fab amino acid sequences, and the crystal structure of the MHC class I and Ig molecules. This model predicts that the complementarity determining regions (CDR) 1 and 2, composed of TCR V alpha and V beta segments, primarily contact residues of the MHC alpha helices, whereas V/J alpha and V/D/J beta junctional regions (the CDR3 equivalent) contact the peptide in the MHC binding groove. Because polymorphism in MHC proteins is limited relative to the enormous diversity of antigenic peptides, the TCR may have evolved to position the highly diverse junctional residues (CDR3), where they have maximal contact with antigen bound in the MHC peptide groove. Here, we demonstrate a definitive association between CDR3 sequences in both TCR alpha and beta chains, and differences in recognition of antigen fine specificity using a panel of I-Ed-restricted, myoglobin-reactive T cell clones. Acquisition of these data relied in part upon a modification of the polymerase chain reaction that uses a degenerate, consensus primer to amplify TCR alpha chains without foreknowledge of the V alpha segments they utilize.

scholarly journals Lymphocyte proliferation in mice congenitally deficient in T-cell receptor alpha beta + cells.

1994 ◽  
Vol 91 (25) ◽  
pp. 11948-11952 ◽  
Author(s):  
J. L. Viney ◽  
L. Dianda ◽  
S. J. Roberts ◽  
L. Wen ◽  
C. A. Mallick ◽  
...  
Keyword(s):  
T Cell ◽  
Beta Cells ◽  
T Cell Receptor ◽  
Lymphocyte Proliferation ◽  
Cell Receptor ◽  
Receptor Alpha ◽  
Alpha Beta ◽  
Cell Receptor Alpha

scholarly journals Validation of a Combined Transcriptome and T Cell Receptor Alpha/Beta (TRA/TRB) Repertoire Assay at the Single Cell Level for Paucicellular Samples

2020 ◽  
Vol 11 ◽  
Author(s):  
Nicolle H. R. Litjens ◽  
Anton W. Langerak ◽  
Amy C. J. van der List ◽  
Mariska Klepper ◽  
Maaike de Bie ◽  
...  
Keyword(s):  
T Cell ◽  
Single Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Single Cell Level ◽  
Cell Level ◽  
Receptor Alpha ◽  
Alpha Beta ◽  
Cell Receptor Alpha

Depletion of T-cell receptor alpha/beta and CD19 positive cells from apheresis products with the CliniMACS device

Cytotherapy ◽  
2013 ◽  
Vol 15 (10) ◽  
pp. 1253-1258 ◽  
Author(s):  
Michael Schumm ◽  
Peter Lang ◽  
Wolfgang Bethge ◽  
Christoph Faul ◽  
Tobias Feuchtinger ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Receptor Alpha ◽  
Alpha Beta ◽  
Cell Receptor Alpha

scholarly journals The T-cell receptor alpha, beta and gamma polymorphism in Japanese

1989 ◽  
Vol 34 (4) ◽  
pp. 269-277
Author(s):  
Juan M. R. Aparicio ◽  
Akemi Wakisaka ◽  
Akio Takada ◽  
Nobuo Matsuura ◽  
Takashi Yoshiki
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Receptor Alpha ◽  
Alpha Beta ◽  
Cell Receptor Alpha

scholarly journals Temporal and lineage-specific control of T cell receptor alpha/delta gene rearrangement by T cell receptor alpha and delta enhancers.

1994 ◽  
Vol 179 (6) ◽  
pp. 1913-1921 ◽  
Author(s):  
P Lauzurica ◽  
M S Krangel
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Gene Rearrangement ◽  
Cell Subset ◽  
Cell Receptor ◽  
Receptor Alpha ◽  
Specific Step ◽  
Delta Gene ◽  
Alpha Beta ◽  
Cell Receptor Alpha

To analyze the regulation of gene rearrangement at the T cell receptor (TCR) alpha/delta locus during T cell development, we generated transgenic mice carrying a human TCR delta gene minilocus. We previously showed that the presence of the TCR delta enhancer (E delta) within the J delta 3-C delta intron was required to activate a specific step (V-D to J) of transgene rearrangement, and that rearrangement was activated equivalently in the precursors of alpha beta and gamma delta T cells. To further explore the role of transcriptional enhancers in establishing the developmental pattern of gene rearrangement at the TCR alpha/delta locus, we substituted the TCR alpha enhancer (E alpha) in place of E delta within the transgenic minilocus. We found that V-D-J rearrangement of the E alpha+ minilocus was restricted to the alpha beta T cell subset. Further, we found that although V-D-J rearrangement of the E delta+ minilocus was initiated in the fetal thymus by day 14.5, V-D-J rearrangement of the E alpha+ minilocus did not occur until fetal day 16.5. Finally, whereas V-D-J rearrangement of the E delta+ minilocus is essentially completed within the triple negative population of postnatal thymocytes, V-D-J rearrangement of the E alpha+ minilocus is only initiated late within this population. Since the properties of minilocus rearrangement under the control of E delta and E alpha parallel the properties of V delta-D delta-J delta and V alpha-J alpha rearrangement at the endogenous TCR alpha/delta locus, we conclude that these enhancers play an important role in orchestrating the developmental program of rearrangements at this locus.

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