Filgrastim Restores Interleukin‐2 Production in Blood from Patients with Advanced Human Immunodeficiency Virus Infection
Author(s) -
Thomas Härtung,
David Pitrak,
MaryAnn Foote,
Edward Shatzen,
Stephen C. Verral,
Albrecht Wendel
Publication year - 1998
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/515338
Subject(s) - filgrastim , immunology , cytokine , ex vivo , medicine , tumor necrosis factor alpha , in vivo , neutropenia , biology , toxicity , microbiology and biotechnology
Filgrastim induces lymphocytosis, including all T cell subsets, and increased ex vivo interleukin (IL)-2 release as well as lymphocyte proliferation. Since Filgrastim is increasingly used in patients with human immunodeficiency virus (HIV) infection, the effect of Filgrastim on ex vivo cytokine production was determined. Whole blood from 8 healthy volunteers, 5 high-risk volunteers, and 31 HIV-infected outpatients was assayed for cytokine production in response to endotoxin (LPS) or staphylococcal enterotoxin B (SEB) in the presence or absence of 100 ng/mL Filgrastim. LPS-inducible blood cytokine release of HIV-infected patients was not different from that of normal or high-risk volunteers. The suppressive effect of Filgrastim on LPS-inducible blood tumor necrosis factor-alpha and interferon-gamma formation in normal volunteers was not found in HIV-infected patients. Patients with advanced HIV infection showed reduced IL-2 and IL-4 release in the presence of SEB. In the presence of Filgrastim, IL-2 production was partially restored.
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