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Lymphokine-dependent proliferation of T-lymphoid cells: regulated responsiveness and role in vivo.
Boothby M, Mora AL, Stephenson LM
(2001) Crit Rev Immunol 21: 487-522
MeSH Terms: Animals, Cell Division, Hematopoietic Cell Growth Factors, Humans, Interleukin-15, Interleukin-2, Interleukin-4, Interleukin-7, Ligands, Lymphocytes, Lymphokines, Receptors, Antigen, T-Cell, Receptors, Antigen, T-Cell, alpha-beta, Receptors, Antigen, T-Cell, gamma-delta, Receptors, Interleukin-2, Receptors, Interleukin-4, Receptors, Interleukin-7, Signal Transduction, T-Lymphocytes
Show Abstract · Added December 10, 2013
The discovery of lymphokines stemmed from their ability to promote T-lymphocyte proliferation in vitro. Even after 20 years of intensive investigation, crucial aspects remain to be clarified about the role of specific lymphokines in T-cell proliferation and the biochemical mechanisms by which they play these roles, particularly in vivo. The present review focuses on conventional populations of TCR(alpha)beta T cells. Older findings and new insights into the function of specific lymphokines in T-lymphocyte proliferation in vivo are summarized along with unanswered questions raised by these observations. Vital contributions of lymphokines to clonal proliferation arise from two processes: the protection of cells against apoptosis and the activation of cell cycling. Findings are underscored indicating that the activity of a particular lymphokine depends on the subset of T cells (CD4 vs. CD8; naive vs. memory) to which it binds, and that point to potential pitfalls of extrapolating from tissue culture-adapted models to the regulation of T cells in vivo. After summaries of signaling mechanisms related to the proliferative activity of lymphokines, recent findings are highlighted suggesting that such signaling is a regulated and plastic process rather than one fixed schema of action.
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19 MeSH Terms
Selective regulation of Bcl-XL by a Jak kinase-dependent pathway is bypassed in murine hematopoietic malignancies.
Packham G, White EL, Eischen CM, Yang H, Parganas E, Ihle JN, Grillot DA, Zambetti GP, Nuñez G, Cleveland JL
(1998) Genes Dev 12: 2475-87
MeSH Terms: Animals, Apoptosis, Base Sequence, Cell Transformation, Neoplastic, Gene Expression Regulation, Neoplastic, Hematopoietic Cell Growth Factors, Janus Kinase 2, Leukemia, Myeloid, Leukemia, T-Cell, Mice, Molecular Sequence Data, Mutagenesis, Insertional, Protein-Tyrosine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-bcl-2, Retroviridae, Sequence Alignment, Tumor Cells, Cultured, bcl-X Protein
Show Abstract · Added March 5, 2014
Bcl-2 family proteins are key regulators of apoptosis and function as cell death antagonists (e.g., Bcl-2, Bcl-XL, and Mcl-1) or agonists (e.g., Bax, Bad, and Bak). Here we report that among the Bcl-2 family of proteins tested (Bcl-2, Bcl-XL, Mcl-1, Bax, Bad, and Bak), Bcl-XL was unique in that its protein levels were tightly regulated by hemopoietins in both immortal and primary myeloid progenitors. Investigating signaling pathways utilized by cytokine receptors established that the regulation of Bcl-XL protein levels is mediated by the Jak kinase pathway and is independent of other signaling effectors including STATs, PI-3' kinase, and Ras. Moreover, we provide the first direct evidence that Bcl-X is altered in cancer, because bcl-X expression was activated selectively by retroviral insertions in murine myeloid and T-cell hemopoietic malignancies. Tumors harboring bcl-X insertions had altered bcl-X RNAs, expressed elevated levels of Bcl-XL protein, and lacked the requirements for cytokines normally essential for cell survival. Finally, overexpression of Bcl-XL effectively protected IL-3-dependent myeloid cells from apoptosis following removal of trophic factors. Therefore, Bcl-XL functions as a key cytokine regulated anti-apoptotic protein in myelopoiesis and contributes to leukemia cell survival.
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19 MeSH Terms
Human thymic epithelial cells produce granulocyte and macrophage colony-stimulating factors.
Le PT, Kurtzberg J, Brandt SJ, Niedel JE, Haynes BF, Singer KH
(1988) J Immunol 141: 1211-7
MeSH Terms: Animals, Bone Marrow Cells, Cell Differentiation, Cell Line, Cell-Free System, Child, Chromatography, Ion Exchange, Colony-Forming Units Assay, Colony-Stimulating Factors, Epithelial Cells, Epithelium, Granulocyte Colony-Stimulating Factor, Granulocyte-Macrophage Colony-Stimulating Factor, Growth Substances, Hematopoietic Cell Growth Factors, Humans, Immunoassay, Leukemia, Myeloid, Acute, Mice, Mice, Inbred BALB C, RNA, Thymus Gland
Show Abstract · Added March 5, 2014
The development of culture conditions for growing normal human thymic epithelial (TE) cells free from contamination with other stromal cells has allowed us to identify and characterize TE cell-derived cytokines. In this study, we report that cultured human TE cells produced CSF that supported the growth of clonal hematopoietic progenitor cells in the light density fraction of human bone marrow cells. Thymic epithelial supernatants (TES) induced growth of granulocyte/macrophage colonies (CFU-GM), mixed granulocyte/erythrocyte/monocyte/megakaryocyte colonies (CFU-GEMM), and early burst-forming unit erythroid colonies (BFU-E). In addition, TES induced differentiation of the promyelocyte leukemic cell line HL-60 and stimulated growth of both granulocyte (CFU-G) and monocyte (CFU-M) colonies from murine bone marrow cells. Using anion exchange column chromatography, pluripotent CSF activities in TES were separated and shown to be distinct from an IL-1-like cytokine that has been shown as a TE cell-derived cytokine (TE-IL-1). Colony-stimulating activity supporting the growth of bone marrow CFU-GEMM, BFU-E, and CFU-GM co-eluted at 150 to 180 mM NaCl. A separate peak of CFU-GM-stimulating activity eluted early in the gradient at 20 mM NaCl. In Northern blot analysis of enriched RNA, synthetic oligonucleotide probes complementary to human G-CSF and M-CSF coding sequence each hybridized with a single RNA species of 1.7 and 4.4 kb, respectively. These data suggest that normal human TE cells synthesize G-CSF and M-CSF that promote differentiation of non-lymphoid hematopoietic cell precursors.
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22 MeSH Terms