ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    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
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 2
    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
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...