A T2 cytokine environment may not limit T1 responses in human immunodeficiency virus patients with a favourable response to antiretroviral therapy.

摘要: Low-level production of interferon-γ (IFN-γ) marks human immunodeficiency virus (HIV)-induced and has been ascribed to a bias towards T2 cytokines. This was investigated in two cross-sectional studies HIV patients who were immunodeficient when they began antiretroviral therapy (ART) had stable increases CD4 T-cell counts. Blood leucocytes assessed unstimulated or after stimulation with cytomegalovirus (CMV), anti-CD3 mitogen. IFN-γ interleukin (IL)-5 responses initially by enzyme-linked immunosorbent spot-forming cell assay (ELISPOT) (ELISA). We then adopted sensitive reverse transcription–polymerase chain reaction (RT–PCR) system assess IFN-γ, IL-5, IL-4 IL-4δ2 (an inhibitory splice variant IL-4) mRNA. The results correlated putative serological markers T1 [lymphocyte activation gene-3 (LAG-3), CD26] [CD30, immunoglobulin E (IgE)] cytokine environment. IL-5 IgE levels elevated patients. did not correlate but showed an inverse correlation released culture (P = 0·05). IL-4, mRNA stimulation, where the best predictor 0·006). Weak positive correlations evident between CD30 levels, whilst inversely IL-4δ2, levels. These analyses provide no evidence for relationship patients, suggest that elevation low responses.