Transforming growth factor-β2 induces apoptosis of murine T cell clones without down-regulatingbcl-2 mRNA expression

1994 ◽  
Vol 24 (6) ◽  
pp. 1293-1300 ◽  
Author(s):  
Michael Weller ◽  
Daniel B. Constam ◽  
Ursula Malipiero ◽  
Adriano Fontana
Keyword(s):  
T Cell ◽  
Growth Factor ◽  
Mrna Expression ◽  
Transforming Growth Factor ◽  
T Cell Clones ◽  
Cell Clones ◽  
Transforming Growth Factor Β2

Correlation between mRNA expression of Th1/Th2 cytokines and their specific transcription factors in human helper T‐cell clones

2005 ◽  
Vol 83 (5) ◽  
pp. 536-541 ◽  
Author(s):  
Noriko Kitamura ◽  
Osamu Kaminuma ◽  
Akio Mori ◽  
Tomomi Hashimoto ◽  
Fujiko Kitamura ◽  
...  
Keyword(s):  
Transcription Factors ◽  
T Cell ◽  
Mrna Expression ◽  
Th2 Cytokines ◽  
Helper T Cell ◽  
T Cell Clones ◽  
Cell Clones

scholarly journals Expression of nerve growth factor and nerve growth factor receptor tyrosine kinase Trk in activated CD4-positive T-cell clones

1993 ◽  
Vol 90 (23) ◽  
pp. 10984-10988 ◽  
Author(s):  
P B Ehrhard ◽  
P Erb ◽  
U Graumann ◽  
U Otten
Keyword(s):  
T Cells ◽  
Nerve Growth Factor ◽  
T Cell ◽  
Growth Factor ◽  
Cd4 T Cells ◽  
Cd4 T Cell ◽  
T Cell Clones ◽  
Nerve Growth ◽  
Cell Clones ◽  
Ngf Receptor

Recent evidence suggests that nerve growth factor (NGF), in addition to its neurotrophic functions, acts as an immunomodulator mediating "cross-talk" between neuronal and immune cells, including T lymphocytes. We have analyzed murine CD4+ T-cell clones for their ability to express transcripts encoding NGF, low-affinity NGF receptor, and trk protooncogene, the signal-transducing receptor subunit for NGF. We show that two CD4+ T-helper (Th) clones, Th0-type clone 8/37 and Th2-type clone D10.G4.1, express NGF and Trk mRNA after appropriate activation with mitogen or with antigen and antigen-presenting cells. NGF and trk induction occurred to a similar extent and over a similar time course in activated 8/37 T cells, raising the possibility that NGF and trk genes are under coordinate control. NGF and NGF receptor expression does not seem to be a universal property of all activated CD4+ T cells, since Th1-type clone 9/9 did not express any of the transcripts after either stimulation. The absence of low-affinity NGF receptor mRNA in resting and activated T cells implies that the low-affinity NGF receptor is not involved in NGF signal transduction in CD4+ T cells. Our finding that activated CD4+ T-cell clones not only express Trk but also synthesize and release biologically active NGF implicates NGF as an autocrine and/or paracrine factor in the development and regulation of immune responses.

scholarly journals Latency-Associated Peptide of Transforming Growth Factor β Enhances Mycobacteriocidal Immunity in the Lung duringMycobacterium bovis BCG Infection in C57BL/6 Mice

2000 ◽  
Vol 68 (11) ◽  
pp. 6505-6508 ◽  
Author(s):  
K. A. Wilkinson ◽  
T. D. Martin ◽  
S. M. Reba ◽  
H. Aung ◽  
R. W. Redline ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Growth Factor ◽  
Mrna Expression ◽  
Mycobacterium Bovis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Gamma Interferon ◽  
T Cell Proliferation

ABSTRACT Latency-associated peptide of transforming growth factor β (TGF-β) (LAP) was used to determine whether in vivo modulation of TGF-β bioactivity enhanced pulmonary immunity to Mycobacterium bovis BCG infection in C57BL/6 mice. LAP decreased BCG growth in the lung and enhanced antigen-specific T-cell proliferation and gamma interferon mRNA expression. Thus, susceptibility of the lung to primary BCG infection may be partially mediated by the immunosuppressive effects of TGF-β.

Human CD4+ T cell clones produce and release nerve growth factor and express high-affinity nerve growth factor receptors

1997 ◽  
Vol 100 (3) ◽  
pp. 408-414 ◽  
Author(s):  
Alessandro Lambiase ◽  
Luisa Bracci-Laudiero ◽  
Sergio Bonini ◽  
Stefano Bonini ◽  
Giuseppe Starace ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
T Cell ◽  
Growth Factor ◽  
Growth Factor Receptors ◽  
Cd4 T Cell ◽  
T Cell Clones ◽  
Nerve Growth ◽  
High Affinity ◽  
Cell Clones ◽  
Nerve Growth Factor Receptors

scholarly journals Transforming growth factor-β2 is involved in quantitative genetic variation in thymic involution

Blood ◽  
2006 ◽  
Vol 107 (5) ◽  
pp. 1974-1979 ◽  
Author(s):  
Ritu Kumar ◽  
Jessica C. Langer ◽  
Hans-Willem Snoeck
Keyword(s):  
Genetic Variation ◽  
T Cell ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Inbred Mouse ◽  
Mouse Strains ◽  
Thymic Involution ◽  
Hematopoietic Stem ◽  
Quantitative Genetic ◽  
Transforming Growth Factor Β2

The mechanisms regulating thymic involution are unclear. In inbred mouse strains the rate of thymic involution and the function of the hematopoietic stem cell (HSC) compartment are subject to quantitative genetic variation. We have shown previously that transforming growth factor-β2 (TGF-β2) is a genetically determined positive regulator of HSCs. Here, we demonstrate that genetic variation in the rate of thymic involution correlates with genetic variation in the responsiveness of hematopoietic stem and progenitor cells to TGF-β2. Corroborating these correlations, thymic cellularity and peripheral naive T-cell frequency were higher in old Tgfb2+/- mice than in wild-type littermates. The frequency of early T-cell precursors was increased in Tgfb2+/- mice, suggesting that TGF-β2 affects the earliest stages of T-cell development in old mice. Reciprocal transplantation experiments indicated that TGF-β2 expressed both in the (micro)environment and in the hematopoietic system can accelerate thymic involution; however, the age of the stem cells appeared irrelevant. Thus, although thymic involution is largely determined by the aged environment, TGF-β2 plays a major modulatory role that is subject to genetic variation and is possibly mediated through its regulatory effects on early hematopoiesis.

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