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1.
Mucosal Immunol ; 14(3): 566-573, 2021 05.
Article in English | MEDLINE | ID: mdl-33608656

ABSTRACT

Viral infections with SARS-CoV-2 can cause a multi-facetted disease, which is not only characterized by pneumonia and overwhelming systemic inflammatory immune responses, but which can also directly affect the digestive system and infect intestinal epithelial cells. Here, we review the current understanding of intestinal tropism of SARS-CoV-2 infection, its impact on mucosal function and immunology and summarize the effect of immune-suppression in patients with inflammatory bowel disease (IBD) on disease outcome of COVID-19 and discuss IBD-relevant implications for the clinical management of SARS-CoV-2 infected individuals.


Subject(s)
COVID-19/complications , COVID-19/immunology , Host-Pathogen Interactions/immunology , Immunity, Mucosal , Inflammatory Bowel Diseases/complications , Inflammatory Bowel Diseases/immunology , SARS-CoV-2/physiology , Biomarkers , COVID-19/diagnosis , COVID-19/virology , Humans , Immunity, Innate , Inflammatory Bowel Diseases/diagnosis , Intestinal Mucosa/immunology , Intestinal Mucosa/metabolism , Intestinal Mucosa/pathology , Severity of Illness Index , Symptom Assessment , Viral Tropism , Virus Internalization
2.
Nat Immunol ; 11(11): 1057-62, 2010 Nov.
Article in English | MEDLINE | ID: mdl-20935646

ABSTRACT

After being activated by antigen, helper T lymphocytes switch from a resting state to clonal expansion. This switch requires inactivation of the transcription factor Foxo1, a suppressor of proliferation expressed in resting helper T lymphocytes. In the early antigen-dependent phase of expansion, Foxo1 is inactivated by antigen receptor-mediated post-translational modifications. Here we show that in the late phase of expansion, Foxo1 was no longer post-translationally regulated but was inhibited post-transcriptionally by the interleukin 2 (IL-2)-induced microRNA miR-182. Specific inhibition of miR-182 in helper T lymphocytes limited their population expansion in vitro and in vivo. Our results demonstrate a central role for miR-182 in the physiological regulation of IL-2-driven helper T cell-mediated immune responses and open new therapeutic possibilities.


Subject(s)
Interleukin-2/immunology , MicroRNAs/immunology , T-Lymphocytes, Helper-Inducer/cytology , T-Lymphocytes, Helper-Inducer/immunology , Animals , Arthritis/immunology , Cell Proliferation , Cells, Cultured , Disease Models, Animal , Humans , Mice , Mice, Inbred BALB C , Mice, Inbred C57BL
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