Vukmanović, Stanislav (35552076100)Stanislav (35552076100)VukmanovićVučković, Slavica (7003869325)Slavica (7003869325)VučkovićStošić-Grujičić, Stanislava (7004253020)Stanislava (7004253020)Stošić-GrujičićRamić, Zorica (6603943950)Zorica (6603943950)RamićAbinun, Mario (55880862200)Mario (55880862200)Abinun2025-07-022025-07-021992https://doi.org/10.1016/0090-1229(92)90156-Ihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-0026678471&doi=10.1016%2f0090-1229%2892%2990156-I&partnerID=40&md5=8e75adb9f4f0516c272c610f37784c15https://remedy.med.bg.ac.rs/handle/123456789/14633Stimulation of T-lymphocytes derived from some patients with common variable immunodeficiency (CVID) syndrome results in defective proliferation. The underlying mechanism is related to the inability of stimulated cells to secrete IL-2 while the expression of IL-2 receptor (IL-2R) is normal. We have identified a patient whose peripheral T-cells failed to proliferate and secrete IL-2 upon stimulation. The addition of recombinant IL-2 restored proliferation. The defect did not seem to be caused by accessory cell failure since the patient's adherent cells produced IL-1 and IL-6, and addition of allogeneic irradiated cells did not induce proliferation. Stimulation of CVID T-cells with phorbol esters and Ca2+ ionophore induced both IL-2 secretion and proliferation, indicating the absence of a defect in the transcription and/or translation of the IL-2 gene. The patient's T-cells expressed high levels of CD3. The majority of T-cells expressed the CD38 molecule which is normally found on thymocytes or activated T-cells but not peripheral blood T-cells and HLA-DR, another activation marker. However, CD25 (the IL-2R) and CD1, a marker of more immature thymocytes, were not expressed. Finally, the patient's cells were sensitive to an in vitro corticosteroid treatment. The possibilities that this patient's T-cells represent anergic T-cells or not fully matured thymocytes are discussed. © 1992.