Rotavirus infection causes mesenteric lymph node hypertrophy independently of type I interferon or TNF‐α in mice
| Autor: | Joy Nakawesi, Bengt Johansson-Lindbom, Getachew Muleta Konjit, Dragos-Christian Dasoveanu, Katharina Lahl |
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| Rok vydání: | 2021 |
| Předmět: |
Rotavirus
0301 basic medicine Lymphocyte Immunology Immunity to infection Lymphadenopathy Biology Lymphocyte Activation medicine.disease_cause Rotavirus Infections Muscle hypertrophy Mice 03 medical and health sciences 0302 clinical medicine Immune system medicine Animals Immunology and Allergy Mesentery Lymphocyte Count Basic Type I interferon Lymph node Research Articles Tumor Necrosis Factor-alpha Hypertrophy Acquired immune system TNF‐α 030104 developmental biology medicine.anatomical_structure Lymphatic system TNF-α lymphoid organ hypertrophy Interferon Type I type I interferon Research Article|Basic Tumor necrosis factor alpha Lymphoid organ hypertrophy Lymph Nodes Signal Transduction 030215 immunology |
| Zdroj: | European Journal of Immunology Nakawesi, J, Konjit, G M, Dasoveanu, D C, Johansson-Lindbom, B & Lahl, K 2021, ' Rotavirus infection causes mesenteric lymph node hypertrophy independently of type I interferon or TNF-α in mice ', European Journal of Immunology, vol. 51, no. 5, pp. 1143-1152 . https://doi.org/10.1002/eji.202048990 |
| ISSN: | 1521-4141 0014-2980 |
| DOI: | 10.1002/eji.202048990 |
| Popis: | Lymphoid organ hypertrophy is a characteristic feature of acute infection and is considered to enable efficient induction of adaptive immune responses. Accordingly, oral infection with rotavirus induced a robust increase in cellularity in the mesenteric LNs, whose kinetics correlated with viral load and was caused by halted lymphocyte egress and increased recruitment of cells without altered cellular proliferation. Lymphocyte sequestration and mesenteric LN hypertrophy were independent of type 1 IFN receptor signaling or the continuous presence of TNF‐α. Our results support previous findings that adaptive immunity toward rotavirus is initiated primarily in the mesenteric LNs and show that type I IFN or TNF‐α are not required to coordinate the events involved in the LN response. Lymphoid organ hypertrophy facilitates lymphocyte priming in response to immune activation. We here report that mesenteric LN expansion in response to asymptomatic rotavirus infection in adult mice is independent of type I IFN and TNF‐α and caused both by enhanced recruitment and halted egress of lymphocytes. |
| Databáze: | OpenAIRE |
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