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Blood, 1 December 2004, Vol. 104, No. 12, pp. 3513-3519.
Prepublished online as a Blood First Edition Paper on August 5, 2004; DOI 10.1182/blood-2004-03-0805.
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Submitted March 3, 2004
Accepted July 13, 2004
Establishment of the CD4+ T cell pool in healthy and untreated HIV-1 infected children
Mette D Hazenberg, Sigrid A Otto, Annemarie M Van Rossum, Henriette J Scherpbier, Ronald de Groot, Taco W Kuijpers, Joep M Lange, Dorte Hamann, Rob J de Boer, Jose A Borghans, and Frank Miedema*
Department of Clinical Viro-Immunology, Sanquin Research at CLB and the Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
Department of Pediatrics, Sophia Children's Hospital/Erasmus University Medical Center, Rotterdam, The Netherlands
Department of Pediatrics/ Emma's Children's Hospital, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
Division of Infectious Diseases, Tropical Medicine and AIDS, National AIDS Therapy Evaluation Center (NATEC), and Department of Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
Department of Theoretical Biology, Utrecht University, Utrecht, The Netherlands
Department of Clinical Viro-Immunology, Sanquin Research at CLB and the Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; Department of Human Retrovirology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
* Corresponding author; email: fmiedema{at}azu.nl.
Current understanding of how the T cell pool is established in children, and how this is affected by HIV infection, is limited. It is widely believed that the thymus is the main source for T cells during childhood. Here we show, however, that healthy children had an age-related increase in total body numbers of naive and memory T cells while absolute numbers of T cell receptor excision circles (TRECs) did not increase. This suggests that expansion of the naive T cell pool after birth is more dependent on T cell proliferation than was previously recognized. Indeed, the proportion of dividing naive T cells was high, especially in younger children, which is consistent with expansion through proliferation, in addition to antigen-mediated naive T cell activation leading to formation of the memory T cell pool. In untreated HIV-1 infected children, total body numbers of T cells and TRECs were low and stable, while T cell division levels were significantly higher than in healthy children. We postulate that in HIV-infected children, similar to HIV-infected adults, continuous activation of naive T cells leads to erosion of the naive T cell pool and may be a major factor lowering CD4 T cell numbers.
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