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Clinical and Diagnostic Laboratory Immunology, May 2002, p. 558-561, Vol. 9, No. 3
1071-412X/02/$04.00+0     DOI: 10.1128/CDLI.9.3.558-561.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Levels of Soluble CD40 Ligand (CD154) in Serum Are Increased in Human Immunodeficiency Virus Type 1-Infected Patients and Correlate with CD4+ T-Cell Counts

Nikolaos V. Sipsas,1 Petros P. Sfikakis,2 Athanasios Kontos,1 and Theodore Kordossis1*

Department of Pathophysiology,1 First Department of Propedeutic Medicine, Laikon General Hospital and School of Medicine, National and Kapodistrian University of Athens, Athens, Greece2

Received 8 November 2001/ Returned for modification 10 January 2002/ Accepted 4 February 2002

CD40 ligand (CD40L or CD154) is a costimulatory molecule expressed mainly on activated CD4+ T cells. Concentrations of the soluble form of CD40L (sCD40L) in serum were determined for a cohort of 77 human immunodeficiency virus type 1 (HIV-1)-infected patients before and after initiation of highly active antiretroviral treatment (HAART) by a quantitative enzyme-linked immunosorbent assay. Circulating sCD40L levels were higher by twofold in untreated patients than in healthy controls (means ± standard deviations [SD]: 1.41 ± 1.48 versus 0.69 ± 0.59 ng/ml; P < 0.001). HIV-1-infected patients classified as CD4 T-cell category 1 had significantly higher sCD40L levels than patients classified as CD4 categories 2 and 3 (mean ± SD: 2.08 ± 1.46 ng/ml versus 1.57 ± 1.58 [category 2] and 0.94 ± 1.25 ng/ml [category 3]; P = 0.046), while no correlation with clinical categories A, B, and C was found. Individual serum sCD40L levels correlated with CD4+ T-cell counts (P = 0.039) but not with viral load, gamma globulin levels, or acute-inflammatory-response markers. After 8 to 12 months of HAART, a further threefold increase of serum sCD40L levels, which paralleled the increase of CD4+ T-cell counts, was observed. These novel findings suggest that sCD40L measurement in HIV-1-infected patients could serve as a new surrogate marker useful in the assessment of treatment efficacy, especially in settings where well-equipped laboratories and funding required for CD4+ T-cell count and viral load measurements are not available.


* Corresponding author. Mailing address: Pathophysiology Department, Athens University Medical School, Mikras Asias 75, Athens GR-115 27, Greece. Phone: 3010-746 2669. Fax: 3010-746 2664. E-mail: tkordoss{at}med.uoa.gr.


Clinical and Diagnostic Laboratory Immunology, May 2002, p. 558-561, Vol. 9, No. 3
1071-412X/02/$04.00+0     DOI: 10.1128/CDLI.9.3.558-561.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.




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