Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2007
Adult onset of T-cell deficiency with impaired CD2 expression complicated by Rhodococcus infection: a case report.
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Kittner Jens Martin, Jacobs Roland, Buyny Sabine, Peest Dietrich, Stoll Matthias, Schmidt Reinhold Ernst
Аннотация
BACKGROUND: The functional importance of CD2 in vivo is currently the subject of discussion.
OBJECTIVE: To describe a 47-year-old white man with systemic Rhodococcus infection, a rarely observed opportunistic disease, secondary to severe lymphopenia.
METHODS: We extensively characterized lymphocyte phenotype and function.
RESULTS: Both CD4+ and CD8+ T cells were severely diminished, with a particular reduction in alpha:beta T cells. Human immunodeficiency virus infection was excluded. CD2 expression was decreased not only on T cells but also on nonaffected natural killer cells. Production of interferon-gamma interleukin 2, and tumor necrosis factor a was normal. Neither B-cell numbers nor humoral immune responses were affected. In addition, adhesion molecules CD11a, CD54, and CD154 were normally expressed, as were the costimulatory molecules CD28, CD80, and CD86.
CONCLUSIONS: We hypothesize that prolonged disturbance of CD2 expression led to an acquired severe cellular immunodeficiency. This underlines the importance of CD2 in vivo, where it may play a role in the fine regulation of T-cell proliferation.
OBJECTIVE: To describe a 47-year-old white man with systemic Rhodococcus infection, a rarely observed opportunistic disease, secondary to severe lymphopenia.
METHODS: We extensively characterized lymphocyte phenotype and function.
RESULTS: Both CD4+ and CD8+ T cells were severely diminished, with a particular reduction in alpha:beta T cells. Human immunodeficiency virus infection was excluded. CD2 expression was decreased not only on T cells but also on nonaffected natural killer cells. Production of interferon-gamma interleukin 2, and tumor necrosis factor a was normal. Neither B-cell numbers nor humoral immune responses were affected. In addition, adhesion molecules CD11a, CD54, and CD154 were normally expressed, as were the costimulatory molecules CD28, CD80, and CD86.
CONCLUSIONS: We hypothesize that prolonged disturbance of CD2 expression led to an acquired severe cellular immunodeficiency. This underlines the importance of CD2 in vivo, where it may play a role in the fine regulation of T-cell proliferation.