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Publication
Interleukin-21 (IL-21) Downregulates Dendritic Cell Cytokine Responses to
Helicobacter pylori and Modulates T Lymphocyte IL-17A Expression in Peyer's
Patches during Infection.
Authors Yasmin S, Dixon BREA, Olivares-Villagómez D, Algood HMS
Submitted By Submitted Externally on 11/24/2019
Status Published
Journal Infection and immunity
Year 2019
Date Published 11/1/2019
Volume : Pages 87 : Not Specified
PubMed Reference 31383743
Abstract Interleukin-21 (IL-21), a cytokine produced by many subsets of activated immune
cells, is critical for driving inflammation in several models. Using
Helicobacter pylori infection as a model for chronic mucosal infection, we
previously published that IL-21 is required for the development of gastritis in
response to infection. Concomitant with protection from chronic inflammation, H.
pylori-infected IL-21-/- mice exhibited limited Th1 and Th17 responses in their
gastric mucosa. Here we report that H. pylori-infected IL-21-/- mice express
significantly higher levels of IL-17A than H. pylori-infected wild-type (WT)
mice in the Peyer's patches and mesenteric lymph nodes. This led us to
hypothesize that IL-21 may indirectly regulate H. pylori-specific T cell
responses by controlling dendritic cell (DC) functions in mucosa-associated
lymphoid tissue. It was found that IL-21 treatment reduced the ability of
dendritic cells to produce proinflammatory cytokines in response to H. pylori
While H. pylori increased the expression of costimulatory proteins on DCs, IL-21
reduced the expression of CD40 in the presence of H. pylori Also, Th17 recall
responses were intact when DCs were used as antigen-presenting cells in the
presence of IL-21, but IL-21 did impact the ability of DCs to induce
antigen-specific proliferation. These data suggest that IL-21, while
proinflammatory in most settings, downregulates the proinflammatory cytokine
microenvironment through modulating the cytokine expression of DCs, indirectly
modifying IL-17A expression. Understanding how these proinflammatory cytokines
are regulated will advance our understanding of how and why H. pylori infection
may be tolerated in some individuals while it causes gastritis, ulcers, or
cancer in others.





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