Summary We studied simultaneously Epstein-Barr virus (EBV)-specific CD4+ and CD8 + T cell responses during and after infectious mononucleosis (IM), using a previously described 12-day stimulation protocol with EBNA1 or BZLF1 peptide pools. Effector function of EBV-specific T cells was determined after restimulation by measuring intracellular interferon-g production. During IM, BZLF1-specifc CD4 + T cell responses were dominant compared with CD8 + T cell responses. EBNA1-specific CD4 + and CD8 + T cell responses were low and remained similar for 6 months. However, 6 months after IM, BZLF1-specific CD4 + T cell responses had declined, but CD8 + T cell responses had increased. At diagnosis, EBV-specific CD8 + T cells as studied by human leucocyte antigen class I tetramer staining comprised a tetramer bright CD8 bright population consisting mainly of CD27 + memory T cells and a tetramer dim CD8 dim population consisting primarily of CD27 -effector T cells. The remaining EBV-specific CD8+ T cell population 6 months after the diagnosis of IM consisted mainly of tetramer bright CD8 bright CD27 + T cells, suggesting preferential preservation of memory T cells after contraction of the EBV-specific T cell pool.

SummarySeveral T cell abnormalities have been described in common variable immunodeficiency (CVID), a B cell disorder of mainly unknown origin. A subset of CVID patients suffers from frequent reactivations of herpes viruses. We studied T cell function in CVID [and in a subset of paediatric patients with specific antibody deficiency (SAD)] by measuring T cell proliferation and cytokine production in response to herpes virus-antigens in paediatric CVID patients (n = 9) and paediatric SAD patients (n = 5), in adult CVID patients (n = 14) and in healthy controls. Paediatric CVID patients, but not SAD patients, displayed moderately increased CD8+ T cell proliferation in response to cytomegalovirus, human herpes virus type 6B (HHV6-B) and herpes simplex virus compared to controls. CD8 + T cell responses in adult CVID patients tended to be increased in response to cytomegalovirus and herpes simplex virus. In response to stimulation with herpes virus antigens, the proinflammatory cytokines interleukin (IL)-1b, IL-6, tumour necrosis factor (TNF)-a and interferon inducible protein (IP)-10 were produced. Overall, no major differences were detected in cytokine production upon stimulation between patients and controls, although higher IL-10 and IL-12 production was detected in paediatric patients. In conclusion, cellular immunity against herpes virus antigens appears undisturbed in CVID patients, although defects in subpopulations of CVID patients cannot be excluded.

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