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Type I interferons keep activated T cells alive.

Marrack P, Kappler J, Mitchell T - J. Exp. Med. (1999)

Bottom Line: It was due to direct effects of the IFNs on the T cells and was not mediated by induction of a second cytokine such as interleukin 15.IFN-alpha/beta did not raise the levels of Bcl-2 or Bcl-XL in T cells.Therefore, their activity was distinct from that of members of the interleukin 2 family or CD28 engagement.

View Article: PubMed Central - PubMed

Affiliation: Howard Hughes Medical Institute, Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado 80206, USA. marrackp@njc.org

ABSTRACT
Antigen injection into animals causes antigen-specific T cells to become activated and, rapidly thereafter, die. This antigen-induced death is inhibited by inflammation. To find out how inflammation has this effect, various cytokines were tested for their ability to interfere with the rapid death of activated T cells. T cells were activated in vivo, isolated, and cultured with the test reagents. Two groups of cytokines were active, members of the interleukin 2 family and the interferons (IFNs) alpha and beta. This activity of IFN-alpha/beta has not been described previously. It was due to direct effects of the IFNs on the T cells and was not mediated by induction of a second cytokine such as interleukin 15. IFN-gamma did not slow the death of activated T cells, and therefore the activity of IFN-alpha/beta was not mediated only by activation of Stat 1, a protein that is affected by both classes of IFN. IFN-alpha/beta did not raise the levels of Bcl-2 or Bcl-XL in T cells. Therefore, their activity was distinct from that of members of the interleukin 2 family or CD28 engagement. Since IFN-alpha/beta are very efficiently generated in response to viral and bacterial infections, these molecules may be among the signals that the immune system uses to prevent activated T cell death during infections.

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Both IFN-α and IFN-β affect the survival of activated T  cells. T cells were activated and purified as described in the legend to Fig.  1. The cells were cultured for 24 h in the presence of various concentrations of IFN-α or IFN-β and the percentages of live activated (Vβ8+) T  cells were determined by flow cytometry. Results shown are the mean ±  SE of triplicate cultures.
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Figure 4: Both IFN-α and IFN-β affect the survival of activated T cells. T cells were activated and purified as described in the legend to Fig. 1. The cells were cultured for 24 h in the presence of various concentrations of IFN-α or IFN-β and the percentages of live activated (Vβ8+) T cells were determined by flow cytometry. Results shown are the mean ± SE of triplicate cultures.

Mentions: The extent to which activated T cells died, and therefore to which IFN-α/β rescued them, varied with time in culture and strain of mice. For example, the cultures shown in Fig. 2 were incubated for 20 h and those shown in Fig. 4 were incubated for 24 h, and there was more extensive death in the absence of, and proportional rescue in the presence of, IFN-α/β in the latter experiments than in the former. The mouse strain from which the activated T cells were derived also affected rates of death in vitro. Thus, the activated T cells from 129 mice (Table II) died more slowly than those from C57Bl/10 mice, a difference between 129 and C57Bl/10 T cells that we have consistently observed in many experiments.


Type I interferons keep activated T cells alive.

Marrack P, Kappler J, Mitchell T - J. Exp. Med. (1999)

Both IFN-α and IFN-β affect the survival of activated T  cells. T cells were activated and purified as described in the legend to Fig.  1. The cells were cultured for 24 h in the presence of various concentrations of IFN-α or IFN-β and the percentages of live activated (Vβ8+) T  cells were determined by flow cytometry. Results shown are the mean ±  SE of triplicate cultures.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2192920&req=5

Figure 4: Both IFN-α and IFN-β affect the survival of activated T cells. T cells were activated and purified as described in the legend to Fig. 1. The cells were cultured for 24 h in the presence of various concentrations of IFN-α or IFN-β and the percentages of live activated (Vβ8+) T cells were determined by flow cytometry. Results shown are the mean ± SE of triplicate cultures.
Mentions: The extent to which activated T cells died, and therefore to which IFN-α/β rescued them, varied with time in culture and strain of mice. For example, the cultures shown in Fig. 2 were incubated for 20 h and those shown in Fig. 4 were incubated for 24 h, and there was more extensive death in the absence of, and proportional rescue in the presence of, IFN-α/β in the latter experiments than in the former. The mouse strain from which the activated T cells were derived also affected rates of death in vitro. Thus, the activated T cells from 129 mice (Table II) died more slowly than those from C57Bl/10 mice, a difference between 129 and C57Bl/10 T cells that we have consistently observed in many experiments.

Bottom Line: It was due to direct effects of the IFNs on the T cells and was not mediated by induction of a second cytokine such as interleukin 15.IFN-alpha/beta did not raise the levels of Bcl-2 or Bcl-XL in T cells.Therefore, their activity was distinct from that of members of the interleukin 2 family or CD28 engagement.

View Article: PubMed Central - PubMed

Affiliation: Howard Hughes Medical Institute, Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado 80206, USA. marrackp@njc.org

ABSTRACT
Antigen injection into animals causes antigen-specific T cells to become activated and, rapidly thereafter, die. This antigen-induced death is inhibited by inflammation. To find out how inflammation has this effect, various cytokines were tested for their ability to interfere with the rapid death of activated T cells. T cells were activated in vivo, isolated, and cultured with the test reagents. Two groups of cytokines were active, members of the interleukin 2 family and the interferons (IFNs) alpha and beta. This activity of IFN-alpha/beta has not been described previously. It was due to direct effects of the IFNs on the T cells and was not mediated by induction of a second cytokine such as interleukin 15. IFN-gamma did not slow the death of activated T cells, and therefore the activity of IFN-alpha/beta was not mediated only by activation of Stat 1, a protein that is affected by both classes of IFN. IFN-alpha/beta did not raise the levels of Bcl-2 or Bcl-XL in T cells. Therefore, their activity was distinct from that of members of the interleukin 2 family or CD28 engagement. Since IFN-alpha/beta are very efficiently generated in response to viral and bacterial infections, these molecules may be among the signals that the immune system uses to prevent activated T cell death during infections.

Show MeSH
Related in: MedlinePlus