Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 98, Issue 5, Pages 2688-2693Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.041624998
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Funding
- NCI NIH HHS [CA-42959] Funding Source: Medline
- NIAID NIH HHS [AI07290] Funding Source: Medline
- NLM NIH HHS [LM-04836] Funding Source: Medline
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Thioredoxin (Trx) is an intracellular redox protein with extracellular cytokine-like and chemokine-like activities, We show here that, although plasma Trx levels are unrelated to survival of HIV-infected individuals with CD4 cell counts above 200/mul blood, survival is significantly impaired (P = 0.003) when plasma Trx is chronically elevated in HIV-infected subjects with CD4 T cell counts below this level (i.e., with Centers for Disease Control (CDC)-defined AIDS). Relevant to the mechanism potentially underlying this finding, we also present data from experimental studies in mice showing that elevated plasma Trx efficiently blocks lipopolysaccharide (LPS)-induced chemotaxis, an innate immune mechanism that is particularly crucial when adaptive immunity is compromised. Thus, we propose that elevated plasma Trx in HIV-infected individuals with low CD4 T cell counts directly impairs survival by blocking pathogen-induced chemotaxis, effectively eliminating the last (innate) barrier against establishment of opportunistic and other infections in these immunodeficient individuals.
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