scholarly journals Antigen-specific, I-A-restricted suppressor hybridomas with spontaneous cytolytic activity. Functional properties and lack of rearrangement of the T cell receptor beta chain genes.

1985 ◽  
Vol 162 (3) ◽  
pp. 851-863 ◽  
Author(s):  
C A Blanckmeister ◽  
K Yamamoto ◽  
M M Davis ◽  
G J Hämmerling
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Antigen Receptor ◽  
Cell Receptor ◽  
Cytolytic Activity ◽  
Hybridoma Cells ◽  
Beta Chain ◽  
T Helper ◽  
Killer Cells ◽  
T Killer Cells

T suppressor (Ts) hybridomas were produced by fusion of the III/4 T cell hybridoma with splenic T cells from CBA mice tolerized with subimmunogenic doses of bovine serum albumin (BSA). Both the Ts hybridoma cells and a suppressor factor (TsF) inhibited in an antigen-specific and I-Ak-restricted fashion the in vitro proliferative response of BSA-immunized lymph node cells. In addition to the suppressive activity, the hybridoma lines displayed spontaneous cytotoxicity against various tumor targets. The isolation of Ts subclones that are suppressive but not cytolytic, as well as the existence of the noncytolytic TsF, indicates that suppression of antigen-specific T cell proliferation is not dependent on cytolytic activity. The Ts hybridomas were I-A restricted, as are many T helper cells. Therefore, a potential similarity with respect to antigen receptor genes was expected. Southern blot analysis with a probe specific for genes encoding the beta chain of the T cell receptor on T helper and T killer cells revealed no rearrangement of the beta genes in the Ts cells. The data imply that neither the antigen receptor on the I-A-restricted Ts cells nor the receptor involved in the cytolytic interaction with tumor targets use the same beta chain constant region as T helper and T killer cells.

scholarly journals Lack of gene rearrangement and mRNA expression of the beta chain of the T cell receptor in spontaneous rat large granular lymphocyte leukemia lines.

1985 ◽  
Vol 161 (5) ◽  
pp. 1249-1254 ◽  
Author(s):  
C W Reynolds ◽  
M Bonyhadi ◽  
R B Herberman ◽  
H A Young ◽  
S M Hedrick
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Antigen Receptor ◽  
Cell Receptor ◽  
Large Granular Lymphocyte ◽  
Beta Chain ◽  
T Cell Antigen Receptor ◽  
Cell Antigen Receptor ◽  
Cell Antigen ◽  
Lgl Leukemia

Using the murine cDNA clone for the beta chain of the T cell antigen receptor, we have examined four highly cytotoxic rat large granular lymphocyte (LGL) leukemia lines for the expression of unique rearrangements and mRNA transcription of the genes coding for the T cell antigen receptor. In contrast to normal rat T cells and nine rat T cell lines, the LGL leukemia lines exhibited no detectable gene rearrangements in the beta chain locus after digestion of LGL DNA by four restriction enzymes. Northern blots containing RNA from these LGL tumor lines demonstrated a low level of aberrant or nonrearranged beta chain transcription (less than 10 copies per cell) but virtually no translatable 1.3 kilobase message. These results demonstrate that LGL leukemia lines which mediate both natural killer (NK) and antibody-dependent cell-mediated cytotoxicity (ADCC) activities do not express the beta chain of the T cell receptor. The nature of the NK cell receptor for antigen remains elusive.

scholarly journals Alteration of Interleukin 4 Production Results in the Inhibition of T Helper Type 2 Cell–Dominated Inflammatory Bowel Disease in T Cell Receptor α Chain–Deficient Mice

1999 ◽  
Vol 190 (5) ◽  
pp. 607-616 ◽  
Author(s):  
Hideki Iijima ◽  
Ichiro Takahashi ◽  
Daisuke Kishi ◽  
Jin-Kyung Kim ◽  
Sunao Kawano ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Bowel Disease ◽  
Cell Receptor ◽  
Interleukin 4 ◽  
T Helper ◽  
Inflammatory Bowel ◽  
Α Chain

T cell receptor α chain–deficient (TCR-α−/−) mice are known to spontaneously develop inflammatory bowel disease (IBD). The colitis that develops in these mice is associated with increased numbers of T helper cell (Th)2-type CD4+TCR-ββ (CD4+ββ) T cells producing predominantly interleukin (IL)-4. To investigate the role of these Th2-type CD4+ββ T cells, we treated TCR-α−/− mice with anti–IL-4 monoclonal antibody (mAb). Approximately 60% of TCR-α−/− mice, including those treated with mock Ab and those left untreated, spontaneously developed IBD. However, anti–IL-4 mAb–treated mice exhibited no clinical or histological signs of IBD, and their levels of mucosal and systemic Ab responses were lower than those of mock Ab–treated mice. Although TCR-α−/− mice treated with either specific or mock Ab developed CD4+ββ T cells, only those treated with anti–IL-4 mAb showed a decrease in Th2-type cytokine production at the level of mRNA and protein and an increase in interferon γ–specific expression. These findings suggest that IL-4–producing Th2-type CD4+ββ T cells play a major immunopathological role in the induction of IBD in TCR-α−/− mice, a role that anti–IL-4 mAb inhibits by causing Th2-type CD4+ββ T cells to shift to the Th1 type.

Diagnosis of T-cell lymphoma using beta F1, anti-T-cell receptor beta chain antibody

1989 ◽  
Vol 15 (3) ◽  
pp. 239-247 ◽  
Author(s):  
A. S. Krajewski ◽  
M. W. Myskow ◽  
D. M. Salter ◽  
D. S. Cunningham ◽  
E. F. Ramage
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Cell Lymphoma ◽  
Cell Receptor ◽  
T Cell Lymphoma ◽  
Beta Chain ◽  
T Cell Receptor Beta ◽  
Receptor Beta

scholarly journals T cell receptor beta chain polymorphisms are associated with cystic fibrosis.

1989 ◽  
Vol 26 (7) ◽  
pp. 431-433 ◽  
Author(s):  
S A McMillan ◽  
A J Hill ◽  
C A Graham ◽  
N C Nevin ◽  
A C Fay
Keyword(s):  
Cystic Fibrosis ◽  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Beta Chain ◽  
T Cell Receptor Beta ◽  
Receptor Beta

scholarly journals Two monoclonal rat antibodies with specificity for the beta-chain variable region V beta 6 of the murine T-cell receptor.

1988 ◽  
Vol 85 (20) ◽  
pp. 7695-7698 ◽  
Author(s):  
J. Payne ◽  
B. T. Huber ◽  
N. A. Cannon ◽  
R. Schneider ◽  
M. W. Schilham ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Variable Region ◽  
Cell Receptor ◽  
Beta Chain

Ig alpha and Ig beta are functionally homologous to the signaling proteins of the T-cell receptor

1994 ◽  
Vol 14 (2) ◽  
pp. 1095-1103
Author(s):  
A L Burkhardt ◽  
T Costa ◽  
Z Misulovin ◽  
B Stealy ◽  
J B Bolen ◽  
...  
Keyword(s):  
Signal Transduction ◽  
T Cells ◽  
T Cell ◽  
B Cell ◽  
T Cell Receptor ◽  
Interleukin 2 ◽  
Antigen Receptor ◽  
Cell Receptor ◽  
Antigen Receptors ◽  
Cell Antigen

Signal transduction by antigen receptors and some Fc receptors requires the activation of a family of receptor-associated transmembrane accessory proteins. One common feature of the cytoplasmic domains of these accessory molecules is the presence is at least two YXXA repeats that are potential sites for interaction with Src homology 2 domain-containing proteins. However, the degree of similarity between the different receptor-associated proteins varies from that of T-cell receptor (TCR) zeta and Fc receptor RIIIA gamma chains, which are homologous, to the distantly related Ig alpha and Ig beta proteins of the B-cell antigen receptor. To determine whether T- and B-cell antigen receptors are in fact functionally homologous, we have studied signal transduction by chimeric immunoglobulins bearing the Ig alpha or Ig beta cytoplasmic domain. We found that Ig alpha and Ig beta cytoplasmic domains were able to activate Ca2+ flux, interleukin-2 secretion, and phosphorylation of the same group of cellular substrates as the TCR in transfected T cells. Chimeric proteins were then used to examine the minimal requirements for activation of the Fyn, Lck, and ZAP kinases in T cells. Both Ig alpha and Ig beta were able to trigger Fyn, Lck, and ZAP directly without involvement of TCR components. Cytoplasmic tyrosine residues in Ig beta were required for recruitment and activation of ZAP-70, but these amino acids were not essential for the activation of Fyn and Lck. We conclude that Fyn and Lck are able to recognize a clustered nonphosphorylated immune recognition receptor, but activation of these kinases is not sufficient to induce cellular responses such as Ca2+ flux and interleukin-2 secretion. In addition, the molecular structures involved in antigen receptor signaling pathways are conserved between T and B cells.

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