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 coordinate the events involved in the LN response.
| Original language | English |
|---|---|
| Journal | European Journal of Immunology |
| Volume | 51 |
| Issue number | 5 |
| Pages (from-to) | 1143-1152 |
| ISSN | 0014-2980 |
| DOIs | |
| Publication status | Published - 2021 |
Bibliographical note
Funding Information:We thank the Lahl and Agace laboratories for many fruitful discussions and Dr. Allan Mowat for editing of the manuscript. KL was supported by a Vetenskapsrådet Young Investigator Award (2014‐3595), the Ragnar Söderberg Foundation Fellowship in Medicine, a Lundbeck Foundation Research Fellowship, the Åke Wiberg Foundation, the Carl Trygger Foundation, and the Crafoord Foundation. KL and JN received project funding from the Royal Physiographic Society of Lund. The flow cytometer at Lund University was purchased with funding from the Lundberg Foundation. We thank Dr. Pronk for sharing TNFR1/2 mice. KL was supported by a Vetenskapsrådet Young Investigator Award (2014‐3595), the Ragnar Söderberg Foundation Fellowship in Medicine, a Lundbeck Foundation Research Fellowship, the Åke Wiberg Foundation, the Carl Trygger Foundation, the Apotekare Hedbergs Foundation, and the Crafoord Foundation.
Keywords
- Lymphoid organ hypertrophy
- Rotavirus
- TNF-α
- Type I interferon