Pathobiont-induced suppressive immune imprints thwart T cell vaccine responses

Pathobionts have evolved many strategies to coexist with the host, but how immune evasion mechanisms contribute to the difficulty of developing vaccines against pathobionts is unclear. Meanwhile, Staphylococcus aureus (SA) has resisted human vaccine development to date. Here we show that prior SA exposure induces non-protective CD4<sup>+</sup> T cell imprints, leading to the blunting of protective IsdB vaccine responses. Mechanistically, these SA-experienced CD4<sup>+</sup> T cells express IL-10, which is further amplified by vaccination and impedes vaccine protection by binding with IL-10Rα on CD4<sup>+</sup> T cell and inhibit IL-17A production. IL-10 also mediates cross-suppression of IsdB and sdrE multi-antigen vaccine. By contrast, the inefficiency of SA IsdB, IsdA and MntC vaccines can be overcome by co-treatment with adjuvants that promote IL-17A and IFN-γ responses. We thus propose that IL-10 secreting, SA-experienced CD4<sup>+</sup> T cell imprints represent a staphylococcal immune escaping mechanism that needs to be taken into consideration for future vaccine development.

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Publication Details

Journal
Nature Communications
Published
2024-12-16
DOI
https://doi.org/10.1038/s41467-024-54644-w
Citations
13
Primary Topic
Immune responses and vaccinations
Type
article
Field-Weighted Citation Impact
3.13

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article

Pathobiont-induced suppressive immune imprints thwart T cell vaccine responses

Xin Du, J.R. Caldera, Brian Lin, María Lázaro-Díez et al.
13 citations
Nature Communications
Immune responses and vaccinations
3.13
article

Pathobiont-induced suppressive immune imprints thwart T cell vaccine responses

Xin Du, J.R. Caldera, Brian Lin, María Lázaro-Díez, Cesia Gonzalez, George Y. Liu, April Aralar, Irshad Hajam, Chih‐Ming Tsai, William Duong
article en
13 citations

Abstract

Pathobionts have evolved many strategies to coexist with the host, but how immune evasion mechanisms contribute to the difficulty of developing vaccines against pathobionts is unclear. Meanwhile, Staphylococcus aureus (SA) has resisted human vaccine development to date. Here we show that prior SA exposure induces non-protective CD4<sup>+</sup> T cell imprints, leading to the blunting of protective IsdB vaccine responses. Mechanistically, these SA-experienced CD4<sup>+</sup> T cells express IL-10, which is further amplified by vaccination and impedes vaccine protection by binding with IL-10Rα on CD4<sup>+</sup> T cell and inhibit IL-17A production. IL-10 also mediates cross-suppression of IsdB and sdrE multi-antigen vaccine. By contrast, the inefficiency of SA IsdB, IsdA and MntC vaccines can be overcome by co-treatment with adjuvants that promote IL-17A and IFN-γ responses. We thus propose that IL-10 secreting, SA-experienced CD4<sup>+</sup> T cell imprints represent a staphylococcal immune escaping mechanism that needs to be taken into consideration for future vaccine development.

Nature CommunicationsVol. 15(1)
UC San Diego Health System (US), University of California San Diego (US), Rady Children's Hospital-San Diego (US), Hospital Universitari Germans Trias i Pujol (ES), Quest Diagnostics (United States) (US)
National Institute of Allergy and Infectious Diseases
Good health and well-being
Openalex Percentile: Top 8%
Immune responses and vaccinations
3.13
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