Open AccessCD28 costimulation and T lymphocyte proliferative responses in HIV‐1 infection
Author(s) -
CARLESIMO M.,
PONTESILLI O.,
VARANI A. R.,
BERNARDI M. L.,
MAZZONE A. M.,
ROSSO R.,
GUERRA E. C.,
CASSONE A.,
PAGANELLI R.,
AIUTI F.
Publication year - 1997
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1046/j.1365-2249.1997.4721370.x
Subject(s) - immunology , cd28 , priming (agriculture) , cd3 , biology , antigen , t lymphocyte , immune system , t cell , cd8 , botany , germination
To investigate whether defective costimulatory signals could be involved in the loss of T lymphocyte functions during HIV‐1 infection, we tested the effect of CD28 costimulation on both T cell receptor/CD3 and HIV‐1 antigen‐induced proliferative responses. Although CD3‐mediated responses significantly decreased with more advanced stages of HIV‐1 infection, the ability of potentiating the responses through CD28 costimulation was maintained at all stages and did not differ from that of HIV‐1 − subjects. When CD28 costimulation was studied in lymphocyte cultures stimulated with HIV‐1 gp160 or p24, potentiation was seen only when a significant response was present without additional CD28 triggering, namely in subjects receiving active immunization with recombinant gp160. These results confirm the integrity of the CD28 pathway of costimulation during HIV‐1 infection, and suggest that lymphocytes responding to soluble HIV‐1 antigen are not deleted in HIV‐1‐infected patients, but do not receive significant priming during the natural course of the infection.