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Differential Effects of IL-33 on Anti-Viral Immune Responses in Asthmatic and Healthy Individuals
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A6222 - Differential Effects of IL-33 on Anti-Viral Immune Responses in Asthmatic and Healthy Individuals
Author Block: J. W. Upham, L. Jurak, Y. Xi; Diamantina Institute, Univ of Queensland, Woolloongabba, Australia.
Rationale: Epithelial cell-derived interleukin-33 (IL-33) appears to have an important role in polarizing type 2 immune responses to allergens, though whether IL-33 can also modify the function of migratory immune cells responding to respiratory viruses is not clear. Aim: Examine the effects of IL-33 on anti-viral cellular immunity in asthma, focusing on the two chains of the IL-33 receptor, interleukin 1 receptor like 1 (IL1RL1; also known as ST2) and IL-1 receptor accessory protein (IL1RAP). Methods: Peripheral blood mononuclear cells were isolated from 16 people with mild/moderate allergic asthma and 16 healthy donors, exposed to IL-33 (10ng/ml) and activated with rhinovirus (RV) serotype 16 for 24h. mRNA and protein expression were assessed by qPCR, flow cytometry and/or ELISA. Results: In those with asthma, RV + IL-33 induced greater IL-5 and IL-13 production, whereas in control subjects, IL-33 enhanced IFNγ production. Both RV alone and RV + IL-33 induced upregulation of IL1RL1/ST2 mRNA and surface protein expression in asthma (p=0.013 and p=0.034 respectively), but not in healthy participants. This was due to enhanced IL1RL1/ST2 expression on both type 2 innate lymphoid cells (ILC2) and conventional T-cells, and was associated with lower soluble ST2 concentrations. In contrast, neither RV nor IL-33 had any effect on expression of IL1RAP expression. ILC2 cells were the major source of IL-13 production, whereas natural killer (NK) cells were the predominant source of IFNγ production. Conclusions: These findings suggest dysregulation of the IL-33 receptor IL1RL1/ST2 in asthma, and provide a mechanism by which RV infections might exacerbate type 2 inflammation in an IL-33 rich tissue environment.
Author Block: J. W. Upham, L. Jurak, Y. Xi; Diamantina Institute, Univ of Queensland, Woolloongabba, Australia.
Rationale: Epithelial cell-derived interleukin-33 (IL-33) appears to have an important role in polarizing type 2 immune responses to allergens, though whether IL-33 can also modify the function of migratory immune cells responding to respiratory viruses is not clear. Aim: Examine the effects of IL-33 on anti-viral cellular immunity in asthma, focusing on the two chains of the IL-33 receptor, interleukin 1 receptor like 1 (IL1RL1; also known as ST2) and IL-1 receptor accessory protein (IL1RAP). Methods: Peripheral blood mononuclear cells were isolated from 16 people with mild/moderate allergic asthma and 16 healthy donors, exposed to IL-33 (10ng/ml) and activated with rhinovirus (RV) serotype 16 for 24h. mRNA and protein expression were assessed by qPCR, flow cytometry and/or ELISA. Results: In those with asthma, RV + IL-33 induced greater IL-5 and IL-13 production, whereas in control subjects, IL-33 enhanced IFNγ production. Both RV alone and RV + IL-33 induced upregulation of IL1RL1/ST2 mRNA and surface protein expression in asthma (p=0.013 and p=0.034 respectively), but not in healthy participants. This was due to enhanced IL1RL1/ST2 expression on both type 2 innate lymphoid cells (ILC2) and conventional T-cells, and was associated with lower soluble ST2 concentrations. In contrast, neither RV nor IL-33 had any effect on expression of IL1RAP expression. ILC2 cells were the major source of IL-13 production, whereas natural killer (NK) cells were the predominant source of IFNγ production. Conclusions: These findings suggest dysregulation of the IL-33 receptor IL1RL1/ST2 in asthma, and provide a mechanism by which RV infections might exacerbate type 2 inflammation in an IL-33 rich tissue environment.
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