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Involvement of the 4-1BB/4-1BBL pathway in control of monocyte numbers by invariant NKT cells. | LitMetric

Involvement of the 4-1BB/4-1BBL pathway in control of monocyte numbers by invariant NKT cells.

J Immunol

Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, United Kingdom.

Published: April 2014

AI Article Synopsis

  • 4-1BB is present on iNKT cells, and its role in interactions with monocytes during influenza infection is explored, revealing mixed effects on cell survival and proliferation.
  • When iNKT cells and monocytes are in contact, they promote each other's expression of 4-1BB and 4-1BBL; blocking this pathway leads to increased cell death in both types of cells under resting conditions.
  • However, upon iNKT activation, these cells induce monocyte apoptosis through mechanisms not reliant on 4-1BB/L, suggesting a complex interplay where 4-1BB/L engagement supports survival in some contexts, while activated iNKT cells can reduce monocyte numbers during an immune response.

Article Abstract

4-1BB is expressed on invariant (i)NKT cells, but its role is unclear. We showed previously that iNKT cells are involved in control of monocyte numbers during influenza A virus (IAV) infection and now question the role of the 4-1BB costimulatory pathway in the cross-talk between these cells. We found that iNKT cells and monocytes interact to promote expression of 4-1BB and 4-1BBL, respectively. Blockade of 4-1BB/L pathway under resting coculture conditions increased apoptosis of iNKT cells and monocytes. However, activation of iNKT cells overrides this survival signal, causing marked apoptosis of monocytes independent of 4-1BB/L. Blocking 4-1BBL in alpha-galactosylceramide-activated iNKT-monocyte cocultures reduced iNKT proliferation and abrogated monocytic IL-12 production. In vivo, expression of 4-1BB and 4-1BBL is increased on iNKT cells and Ly6C(hi) monocytes, respectively, during IAV infection, and there were lower frequencies of apoptosing Ly6C(hi) monocytes in the blood of iNKT knockout mice and higher numbers of monocytes in lungs compared with infected wild-type mice. Adoptive transfer of iNKT cells into the lungs of these mice reduced lung Ly6C(hi) monocytes levels, even when iNKT cells were preincubated with 4-1BB blocking Abs. These findings suggest that under resting conditions, 4-1BB/L engagement during iNKT-monocyte interaction promotes survival of these cells. When iNKT cells are activated, whether by alpha-galactosylceramide or during IAV infection, iNKT cells induced apoptosis of monocytes via a 4-1BB/L-independent mechanism, reducing monocyte numbers. 4-1BB/L costimulation amplified monocyte-mediated proliferation of iNKT cells, indirectly providing a method for monocytes to control their own numbers during infection.

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Source
http://dx.doi.org/10.4049/jimmunol.1302385DOI Listing

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