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  • 1
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    Increased osteoclast development after estrogen loss: mediation by interleukin-6 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-03
    Description: Osteoclasts, the cells that resorb bone, develop from hematopoietic precursors of the bone marrow under the control of factors produced in their microenvironment. The cytokine interleukin-6 can promote hematopoiesis and osteoclastogenesis. Interleukin-6 production by bone and marrow stromal cells is suppressed by 17 beta-estradiol in vitro. In mice, estrogen loss (ovariectomy) increased the number of colony-forming units for granulocytes and macrophages, enhanced osteoclast development in ex vivo cultures of marrow, and increased the number of osteoclasts in trabecular bone. These changes were prevented by 17 beta-estradiol or an antibody to interleukin-6. Thus, estrogen loss results in an interleukin-6-mediated stimulation of osteoclastogenesis, which suggests a mechanism for the increased bone resorption in postmenopausal osteoporosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jilka, R L -- Hangoc, G -- Girasole, G -- Passeri, G -- Williams, D C -- Abrams, J S -- Boyce, B -- Broxmeyer, H -- Manolagas, S C -- AI21761/AI/NIAID NIH HHS/ -- AR41313/AR/NIAMS NIH HHS/ -- CA36464/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Jul 3;257(5066):88-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Veterans Affairs Medical Center, Indiana University School of Medicine, Indianapolis 46202.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1621100" target="_blank"〉PubMed〈/a〉
    Keywords: Analysis of Variance ; Animals ; Antibodies, Monoclonal ; Bone Marrow Cells ; Cells, Cultured ; Estradiol/*pharmacology ; Female ; Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology ; Immunoglobulin G ; Interleukin-6/immunology/*physiology ; Mice ; Osteoclasts/*cytology/drug effects ; *Ovariectomy ; Recombinant Proteins/pharmacology ; Spleen/cytology ; Stem Cells/cytology/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Differing lymphokine profiles of functional subsets of human CD4 and CD8 T cell clones (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-11
    Description: Functional subsets of human T cells were delineated by analyzing patterns of lymphokines produced by clones from individuals with leprosy and by T cell clones of known function. CD4 clones from individuals with strong cell-mediated immunity produced predominantly interferon-gamma, whereas those clones that enhanced antibody formation produced interleukin-4. CD8 cytotoxic T cells secreted interferon-gamma. Interleukin-4 was produced by CD8 T suppressor clones from immunologically unresponsive individuals with leprosy and was found to be necessary for suppression in vitro. Both the classic reciprocal relation between antibody formation and cell-mediated immunity and resistance or susceptibility to certain infections may be explained by T cell subsets differing in patterns of lymphokine production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salgame, P -- Abrams, J S -- Clayberger, C -- Goldstein, H -- Convit, J -- Modlin, R L -- Bloom, B R -- AI-07118/AI/NIAID NIH HHS/ -- AI-20111/AI/NIAID NIH HHS/ -- AI-26491/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Oct 11;254(5029):279-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Albert Einstein College of Medicine, New York, NY 10461.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1681588" target="_blank"〉PubMed〈/a〉
    Keywords: Antibody Formation ; *Antigens, CD4 ; *Antigens, CD8 ; CD4-Positive T-Lymphocytes/secretion ; Clone Cells ; Humans ; Interferon-gamma/secretion ; Interleukin-4/secretion ; Interleukins/secretion ; Leprosy/immunology ; Lymphokines/*secretion ; T-Lymphocyte Subsets/*secretion ; T-Lymphocytes/secretion
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    COOH-terminal-modified interleukin-3 is retained intracellularly and stimulates autocrine growth (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-09-29
    Description: Autocrine growth due to dysregulated growth factor production may have a role in the development of neoplasia. Whether autocrine growth is stimulated by growth factor secretion in an autocrine loop or by intracellular binding of the growth factor to a receptor has been unclear. The carboxyl-terminus coding sequence for murine interleukin-3 (IL-3) was extended with an oligonucleotide encoding a four-amino acid endoplasmic reticulum retention signal. IL-3-dependent hematopoietic cells became growth factor-independent when the modified IL-3 gene was introduced by retroviral gene transfer, despite lack of secretion of the modified IL-3. Hence autocrine growth can occur as a result of the intracellular action of a growth factor and this mechanism may be important in neoplastic and normal cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dunbar, C E -- Browder, T M -- Abrams, J S -- Nienhuis, A W -- New York, N.Y. -- Science. 1989 Sep 29;245(4925):1493-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Clinical Hematology Branch, National Heart, Lung, and Blood Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2789432" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Division/drug effects ; Cell Transformation, Neoplastic ; Cells, Cultured ; Clone Cells ; Interleukin-3/genetics/metabolism/*physiology ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Recombinant Fusion Proteins/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Activation of mouse T-helper cells induces abundant preproenkephalin mRNA synthesis (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-09
    Description: Antigenic or mitogenic stimulation of T cells induces the secretion of an array of protein hormones that regulate immune responses. Molecular cloning has contributed strongly to our present understanding of the nature of this regulation. A complementary DNA (cDNA) library prepared from a cloned concanavalin A-activated mouse T-helper cell line was screened for abundant and induction-specific cDNA's. One such randomly chosen cDNA was found to encode mouse preproenkephalin messenger RNA (mRNA). Preproenkephalin mRNA represented about 0.4 percent of the mRNA in the activated cell line but was absent in resting cells of this line. Other induced T-helper cell lines have 0.1 to 0.5 percent of their mRNA as preproenkephalin mRNA. Induced T-helper cell culture supernatants have [Met]enkephalin-immunoreactive material. The production by activated T cells of a peptide neurotransmitter identifies a signal that can potentially permit T cells to modulate the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zurawski, G -- Benedik, M -- Kamb, B J -- Abrams, J S -- Zurawski, S M -- Lee, F D -- New York, N.Y. -- Science. 1986 May 9;232(4751):772-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2938259" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cattle ; Cell Line ; Cloning, Molecular ; DNA/genetics ; Enkephalins/*biosynthesis/genetics ; Humans ; *Lymphocyte Activation ; Mice ; Protein Precursors/*biosynthesis/genetics ; RNA, Messenger/*biosynthesis ; Rats ; T-Lymphocytes, Helper-Inducer/drug effects/metabolism/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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