Library

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
    Electronic Resource
    Electronic Resource
    Oxford, UK; Malden , USA : Blackwell Science Ltd
    Scandinavian journal of immunology 59 (2004), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The purpose of this study was to investigate the effect of splenectomy on cellular immunity. We studied the cellular phenotype and type 1 [interferon-γ, interleukin-2 (IL-2)] and type 2 (IL-4 and IL-10) cytokine-producing peripheral blood CD4+ and CD8+ T lymphocytes in 22 healthy adults who had undergone post-traumatic splenectomy about 1 to 35 years ago. Splenectomy resulted in a long-term reduction of the percentage of CD4+CD45RA+ cells and a late increase of the percentage and absolute numbers of T-cell receptor γ/δ cells. Stimulation with Staphylococcal enterotoxin B resulted in normal IL-2 production by CD4+ T cells, indicating that the naïve cells were not anergic. Splenectomy also resulted in long-term priming of both CD4+ and CD8+ T cells. During the first 8 years, both type 1 and type 2 CD4+ T cells were primed to varying degrees. About 8 years later, the percentage of primed type 2 CD4+ T cells subsided, but that of type 1 CD4+ T cells, although decreased, remained detectable over a longer period. Priming of CD8+ T cells persisted throughout the study period. The long-term priming of type 1 CD4+ and CD8+ T cells, which may result in partial impairment of T-cell functions, may explain reported defects of immune responses to recall antigens in splenectomized individuals. In addition, changes in the profile of primed CD4+ T cells with time may be clinically relevant to relapses in autoimmune thrombocytopenia after splenectomy.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...