scholarly journals Expression of a transgenic T cell receptor beta chain enhances collagen-induced arthritis.

1992 ◽  
Vol 176 (2) ◽  
pp. 381-388 ◽  
Author(s):  
L Mori ◽  
H Loetscher ◽  
K Kakimoto ◽  
H Bluethmann ◽  
M Steinmetz
Keyword(s):  
T Cell ◽  
Cell Clone ◽  
Gene Segment ◽  
Cell Receptor ◽  
Beta Chain ◽  
Collagen Induced Arthritis ◽  
Peripheral Lymph ◽  
T Cell Clone ◽  
T Cell Receptor Beta ◽  
Receptor Beta

SWR/J transgenic (tg) mice were generated expressing the TCR beta chain derived from an anticollagen type II (CII) arthritogenic T cell clone. The SWR/J strain was selected because it is resistant to collagen-induced arthritis (CIA) and lacks the V beta gene segment used by the T cell clone. Expression of the tg beta chain on all thymocytes and peripheral lymph node T cells led to a more efficient anti-CII immune response, but did not confer CIA susceptibility to SWR/J mice. Nevertheless, this tg beta chain enhanced predisposition to CIA as (DBA/1 x SWR) F1 beta tg mice were more susceptible than normal F1 littermates. Our results demonstrate that the expression of the tg beta chain contributes to CIA susceptibility, but by itself it is not sufficient to overcome CIA resistance in the SWR/J strain.

scholarly journals Early expression of a T-cell receptor beta-chain transgene suppresses rearrangement of the V gamma 4 gene segment.

1988 ◽  
Vol 85 (24) ◽  
pp. 9729-9732 ◽  
Author(s):  
H. von Boehmer ◽  
M. Bonneville ◽  
I. Ishida ◽  
S. Ryser ◽  
G. Lincoln ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Gene Segment ◽  
Cell Receptor ◽  
Beta Chain ◽  
Early Expression ◽  
T Cell Receptor Beta ◽  
Receptor Beta

scholarly journals T cell receptor-beta mRNA splicing: regulation of unusual splicing intermediates.

1993 ◽  
Vol 13 (3) ◽  
pp. 1686-1696 ◽  
Author(s):  
L Qian ◽  
L Theodor ◽  
M Carter ◽  
M N Vu ◽  
A W Sasaki ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Splice Site ◽  
Rna Splicing ◽  
Cell Clone ◽  
Cell Receptor ◽  
Mrna Levels ◽  
T Cell Clone ◽  
T Cell Receptor Beta ◽  
Receptor Beta

The expression of functional T cell receptor-beta (TCR-beta) transcripts requires the activation of programmed DNA rearrangement events. It is not clear whether other mechanisms dictate TCR-beta mRNA levels during thymic ontogeny. We examined the potential role of RNA splicing as a regulatory mechanism. As a model system, we used an immature T cell clone, SL12.4, that transcribes a fully rearranged TCR-beta gene but essentially lacks mature 1.3-kb TCR-beta transcripts in the cytoplasm. Abundant TCR-beta splicing intermediates accumulate in the nucleus of this cell clone. These splicing intermediates result from inefficient or inhibited excision of four of the five TCR-beta introns; the only intron that is efficiently spliced is the most 5' intron, IVSL. The focal point for the regulation appears to be IVS1C beta 1 and IVS2C beta 1, since unusual splicing intermediates that have cleaved the 5' splice site but not the 3' splice site of these two introns accumulate in vivo. The block in 3' splice site cleavage is of interest since sequence analysis reveals that these two introns possess canonical splice sites. A repressional mechanism involving a labile repressor protein may be responsible for the inhibition of RNA splicing since treatment of SL12.4 cells with the protein synthesis inhibitor cycloheximide reversibly induces a rapid and dramatic accumulation of fully spliced TCR-beta transcripts in the cytoplasm, concomitant with a decline in TCR-beta pre-mRNAs in the nucleus. This inducible system may be useful for future studies analyzing the underlying molecular mechanisms that regulate RNA splicing.

T cell receptor-beta mRNA splicing: regulation of unusual splicing intermediates

1993 ◽  
Vol 13 (3) ◽  
pp. 1686-1696
Author(s):  
L Qian ◽  
L Theodor ◽  
M Carter ◽  
M N Vu ◽  
A W Sasaki ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Splice Site ◽  
Rna Splicing ◽  
Cell Clone ◽  
Cell Receptor ◽  
Mrna Levels ◽  
T Cell Clone ◽  
T Cell Receptor Beta ◽  
Receptor Beta

The expression of functional T cell receptor-beta (TCR-beta) transcripts requires the activation of programmed DNA rearrangement events. It is not clear whether other mechanisms dictate TCR-beta mRNA levels during thymic ontogeny. We examined the potential role of RNA splicing as a regulatory mechanism. As a model system, we used an immature T cell clone, SL12.4, that transcribes a fully rearranged TCR-beta gene but essentially lacks mature 1.3-kb TCR-beta transcripts in the cytoplasm. Abundant TCR-beta splicing intermediates accumulate in the nucleus of this cell clone. These splicing intermediates result from inefficient or inhibited excision of four of the five TCR-beta introns; the only intron that is efficiently spliced is the most 5' intron, IVSL. The focal point for the regulation appears to be IVS1C beta 1 and IVS2C beta 1, since unusual splicing intermediates that have cleaved the 5' splice site but not the 3' splice site of these two introns accumulate in vivo. The block in 3' splice site cleavage is of interest since sequence analysis reveals that these two introns possess canonical splice sites. A repressional mechanism involving a labile repressor protein may be responsible for the inhibition of RNA splicing since treatment of SL12.4 cells with the protein synthesis inhibitor cycloheximide reversibly induces a rapid and dramatic accumulation of fully spliced TCR-beta transcripts in the cytoplasm, concomitant with a decline in TCR-beta pre-mRNAs in the nucleus. This inducible system may be useful for future studies analyzing the underlying molecular mechanisms that regulate RNA splicing.

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 Terminal deoxynucleotidyl transferase expression can precede T cell receptor beta chain and gamma chain rearrangement in T cell acute lymphoblastic leukemia

Blood ◽  
1987 ◽  
Vol 69 (1) ◽  
pp. 356-360
Author(s):  
JM Greenberg ◽  
JH Kersey
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
T Cell Receptor ◽  
Lymphoblastic Leukemia ◽  
Cell Receptor ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Beta Chain ◽  
Gamma Chain ◽  
T Cell Receptor Beta ◽  
Receptor Beta

The nuclear enzyme terminal deoxynucleotidyl transferase (TdT) is thought to contribute to the diversity of certain immunoglobulin and T cell receptor gene rearrangements through the addition of random nucleotides at their variable (V)-joining (J) region junctions. An acute lymphoblastic leukemia (ALL) with an immature T cell phenotype (CD7+, CD5+, CD1+/-, CD2+/-, CD3-, CD4-, CD8-) was found to be TdT+ with germline immunoglobulin heavy chain, T cell receptor beta chain, and T cell gamma chain genes. The data indicate that TdT expression can precede T gamma and T beta rearrangement during T lymphoid ontogeny consistent with its proposed association with the T cell receptor rearrangement process. Southern analysis of certain cases of T-ALL may not result in the detection of a monoclonal population of cells.

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