The control of class II expression on T cells is independent of the regulation of Tac and the induction of proliferation.
In order to define the association between class II expression and other markers of T cell activation we tested the ability of various modes of stimulation to induce the expression of class II, Tac, and to stimulate proliferation. Stimulation of T cells with phytohaemagglutinin (PHA) in the presence of accessory cells strongly induced proliferation, Tac and the class II antigen DR. When purified T cells without accessory cells were stimulated with the phorbol ester, PdB, and the calcium ionophore, ionomycin, strong proliferation and Tac expression were induced, but only low levels of surface class II were observed. In contrast, stimulation of the same cells with PHA resulted in weak proliferation, strong Tac, but again low class II levels. The addition of PdB to the PHA increased the proliferative response, but did not affect Tac expression, which remained high, or class II expression, which remained low. Subsequent culture in conditioned medium of purified T cells which had been activated with either PdB and ionomycin or with PHA resulted in increased surface class II levels in both cases. Additional experiments suggested that neither IL-2, IL-4, nor interferon-gamma (IFN-gamma) alone was responsible. These results demonstrate that class II expression can be separated from the induction of proliferation and the upregulation of Tac and that the mode of T cell stimulation influences the resulting activation pathway. Furthermore, they suggest that the control of class II expression on T cells is more tightly regulated than it is on other cells.
Salvadori
S
S
Department of Medicine and Microbiology, Mt. Sinai School of Medicine, New York, NY 10029.
Pizzimenti
A
A
Cohen
S
S
Zier
K S
KS
D000945:Antigens, Differentiation, T-Lymphocyte / Q000502:physiology; D017252:CD3 Complex; D002455:Cell Division / Q000502:physiology; D005434:Flow Cytometry; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology*; D006684:HLA-DR Antigens / Q000096:biosynthesis*; D006801:Humans; D066298:In Vitro Techniques; D007371:Interferon-gamma / Q000494:pharmacology; D007376:Interleukin-2 / Q000494:pharmacology; D015847:Interleukin-4 / Q000494:pharmacology; D015759:Ionomycin / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000502:physiology; D010703:Phorbol Esters / Q000494:pharmacology; D010835:Phytohemagglutinins; D011948:Receptors, Antigen, T-Cell / Q000502:physiology; D015375:Receptors, Interleukin-2 / Q000096:biosynthesis*; D013601:T-Lymphocytes / Q000378:metabolism*
D000945:Antigens, Differentiation, T-Lymphocyte; D017252:CD3 Complex; D006684:HLA-DR Antigens; D007376:Interleukin-2; D010703:Phorbol Esters; D010835:Phytohemagglutinins; D011948:Receptors, Antigen, T-Cell; D015375:Receptors, Interleukin-2; D015847:Interleukin-4; D015759:Ionomycin; D007371:Interferon-gamma