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IL-21-dependent Ly6C+Ly6G+CD4+ T cells found in lung enhance macrophages function against Actinobacillus pleuropneumoniae infection in mice
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IL-21-dependent Ly6C+Ly6G+CD4+ T cells found in lung enhance macrophages function against Actinobacillus pleuropneumoniae infection in mice
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IL-21-dependent Ly6C+Ly6G+CD4+ T cells found in lung enhance macrophages function against Actinobacillus pleuropneumoniae infection in mice
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Journal Article
IL-21-dependent Ly6C+Ly6G+CD4+ T cells found in lung enhance macrophages function against Actinobacillus pleuropneumoniae infection in mice
2025
Overview
IL-21/IL-21R signaling is crucial in various immune diseases and cellular development, however, its role in bacterial pneumonia remains unclear. Here, IL-21R knockout (IL-21R
−
/−
) mice were more susceptible to
Actinobacillus pleuropneumoniae
(APP) than wild-type (WT) mice. High-dimensional mass cytometry analysis revealed that IL-21R deficiency inhibited neutrophil activation, decreased the numbers of monocytes and proinflammatory macrophages, and augmented the defective CD3
low
T cells in the lungs. Intracellular cytokine staining showed decreased IFN-γ/TNF-α/IL-6 production in IL-21R
−
/−
mice, particularly in CD8⁺ T cells. Furthermore, a previously unrecognized Ly6C
+
Ly6G
+
CD4
+
T cell subset emerged only in the lungs of WT mice post-APP infection, which was in an activated status with stronger secretion capacities of IL-10, IL-21, granzyme B, and perforin by flow cytometry. These cells polarized macrophages into M2- or M1- phenotype without/with infection, respectively, and enhanced proliferation, phagocytosis, and macrophage extracellular traps/ROS-mediated bactericidal activity of macrophages against-APP,
Klebsiella pneumoniae
, or
Escherichia coli
infection. Thus, our study demonstrated that IL-21 drives the differentiation of neutrophils, monocytes, and macrophages into pro-inflammatory subsets. IL-21-induced Ly6C
+
Ly6G
+
CD4
+
T cells cooperate with macrophages to enhance bacterial clearance, providing a promising target for preventing bacterial pneumonia.
Publisher
Nature Publishing Group UK,Springer Nature B.V,Nature Publishing Group
Subject
