作者: M Baseler , G Pantaleo , H C Lane , S Koenig , A S Fauci
DOI:
关键词: Antigen 、 Population 、 Clonogenic assay 、 T cell 、 Cell 、 Immunology 、 IL-2 receptor 、 Biology 、 CD3 、 CD8 、 Molecular biology
摘要: This study examines the potential mechanism(s) responsible for defective clonability of CD8+ T lymphocytes in patients with AIDS. By combined use one- and two-color fluorescence cytofluorometry we have shown an increase number circulating DR+ cells due to expression DR on a relatively large proportion (one-third CD3+ cells), majority them belonging subset. In addition, CD8+DR+ AIDS did not express CD25 Ag (the receptor IL-2), surface marker generally expressed normal activated lymphocytes. Sorted CD8+DR- cell populations were analyzed comparatively their ability proliferate response different stimuli, including anti-CD3, anti-CD2, alone or combination anti-CD28 mAb mitogens such as PHA, PMA. We demonstrated that severely proliferative triggering via these major pathways activation even when exogenous source IL-2 IL-4 was added microcultures 24 h after initiating cultures. contrast, showed significant proliferation stimuli strongly enhanced by addition IL-4. At end stimulation period proliferating expression. Only 1 10% antigen compared 40 50% cells. The defect further confirmed experiments performed at clonal level. analysis frequency lymphocyte-precursors both subsets clonogenic could be part ascribed Five percent 25% Finally, VLA-2 Ag, chronic state activation, CD3+DR+CD25- (50 80% analyzed) Ag.(ABSTRACT TRUNCATED AT 400 WORDS)