Expression of adhesion molecules and CD28 on T lymphocytes during human immunodeficiency virus infection

Suk W. Park, Walter Royal, Richard D. Semba, Gordon W. Wiegand, Diane E. Griffin

Research output: Contribution to journalArticlepeer-review

Abstract

Adhesion molecules. which play a major role in lymphocyte circulation, have not been well characterized in human immunodeficiency virus (HIV) infection, T-lymphocyte populations, including CD3, CD4, CD28, and adhesion molecules (L selectin, LFA-1, VLA-4, and ICAM-1) were measured by flow cytometry in a cross-sectional study of 100 HIV-infected and 49 HIV-seronegative adults. HIV-infected adults had lower numbers of CD3+ lymphocytes expressing L selectin (P < 0.0001) and VLA-4 (P < 0.01) and higher numbers of CD3+ lymphocytes expressing LFA-1(bright) (P < 0.002) than did HIN-negative adults. By CD4+-lymphocyte count category (>500, 200 to 500, or <200 cells/μl), HIV-infected adults with more advanced disease had lower percentages of CD3+ lymphocytes expressing L selectin and VLA-4 and higher percentages of CD3+ lymphocytes expressing LFA-1. The percentages of CD3+ CD28+ lymphocytes and of CD3+ L selectin+ lymphocytes were positively correlated (Spearman coefficient = 0.86; P < 0.0001), and the percentage of CD3+ CD28+ lymphocytes and the CD3+ LFA-1(bright) lymphocyte/CD3+ LFA-1(dim) lymphocyte ratio were negatively correlated (Spearman coefficient = -0.92; P < 0.00001). The results of this study suggest that HIV infection is associated with altered expression of adhesion molecules.

Original languageEnglish (US)
Pages (from-to)583-587
Number of pages5
JournalClinical and Diagnostic Laboratory Immunology
Volume5
Issue number4
DOIs
StatePublished - 1998

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Clinical Biochemistry
  • Microbiology (medical)

Fingerprint Dive into the research topics of 'Expression of adhesion molecules and CD28 on T lymphocytes during human immunodeficiency virus infection'. Together they form a unique fingerprint.

Cite this