Rotavirus infection causes mesenteric lymph node hypertrophy independently of type I interferon or TNF-α in mice

Joy Nakawesi, Getachew Muleta Konjit, Dragos Christian Dasoveanu, Bengt Johansson-Lindbom, Katharina Lahl

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskriftPeer review

1 Citering (SciVal)

Sammanfattning

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.

Originalspråkengelska
Sidor (från-till)1143-1152
Antal sidor10
TidskriftEuropean Journal of Immunology
Volym51
Utgåva5
DOI
StatusPublished - 2021

Ämnesklassifikation (UKÄ)

  • Immunologi inom det medicinska området

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