Rotavirus infection causes mesenteric lymph node hypertrophy independently of type I interferon or TNF-α in mice
(2021) In European Journal of Immunology 51(5). p.1143-1152- Abstract
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... (More)
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.
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- author
- Nakawesi, Joy LU ; Konjit, Getachew Muleta LU ; Dasoveanu, Dragos Christian ; Johansson-Lindbom, Bengt LU and Lahl, Katharina LU
- organization
- publishing date
- 2021
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- lymphoid organ hypertrophy, rotavirus, TNF-α, type I interferon
- in
- European Journal of Immunology
- volume
- 51
- issue
- 5
- pages
- 10 pages
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- scopus:85099809833
- pmid:33354817
- ISSN
- 0014-2980
- DOI
- 10.1002/eji.202048990
- language
- English
- LU publication?
- yes
- id
- d199ddc2-d694-4f5b-917a-12c09e33bc59
- date added to LUP
- 2021-12-09 13:25:19
- date last changed
- 2024-06-15 22:22:02
@article{d199ddc2-d694-4f5b-917a-12c09e33bc59,
abstract = {{<p>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.</p>}},
author = {{Nakawesi, Joy and Konjit, Getachew Muleta and Dasoveanu, Dragos Christian and Johansson-Lindbom, Bengt and Lahl, Katharina}},
issn = {{0014-2980}},
keywords = {{lymphoid organ hypertrophy; rotavirus; TNF-α; type I interferon}},
language = {{eng}},
number = {{5}},
pages = {{1143--1152}},
publisher = {{John Wiley & Sons Inc.}},
series = {{European Journal of Immunology}},
title = {{Rotavirus infection causes mesenteric lymph node hypertrophy independently of type I interferon or TNF-α in mice}},
url = {{http://dx.doi.org/10.1002/eji.202048990}},
doi = {{10.1002/eji.202048990}},
volume = {{51}},
year = {{2021}},
}