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Recombinant interleukin‐16 selectively modulates surface receptor expression and cytokine release in macrophages and dendritic cells
Author(s) -
Emmanuel Hermann,
Edith Darcissac,
Thierry Idziorek,
A Capron,
George M. Bahr
Publication year - 1999
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1999.00786.x
Subject(s) - cd86 , cd80 , chemokine , biology , il 2 receptor , microbiology and biotechnology , cytokine , dendritic cell , monocyte , antigen presenting cell , immune system , immunology , cd40 , t cell , cytotoxic t cell , in vitro , biochemistry
Interleukin‐16 (IL‐16), a natural ligand for the CD4 receptor , has been found to modulate T‐lymphocyte function and to inhibit human immunodeficiency virus type 1 (HIV‐1) replication. Antigen‐presenting cells (APC), including macrophages and dendritic cells, are known to express functional surface CD4 molecules, to be susceptible to HIV‐1 infection and to play a critical role in different immune processes. Therefore, we evaluated the ability of recombinant IL‐16 (rIL‐16) to regulate receptor expression and cytokine release in monocyte‐derived macrophages (MDM) and monocyte‐derived dendritic cells (MDDC). Recombinant IL‐16 was found to up‐regulate CD25 and CD80 but to down‐regulate CD4 and CD86 surface expression in MDM cultures. However, no change could be observed on the level of CD4, CD80 and CD86 expression in IL‐16‐stimulated MDDC, although a significant up‐regulation of CD25 and CD83 was consistently detected. Furthermore, the level of gene expression of the chemokine receptors CCR5 and CXCR4 was significantly reduced in rIL‐16‐treated MDM and costimulation with IL‐2 did not modify the activity of the recombinant cytokine. The effects on chemokine receptor gene expression were less evident in MDDC and only a transient down‐regulation of weak intensity could be detected following stimulation with rIL‐16. Analysis of supernatants from rIL‐16‐stimulatedcultures revealed a different profile of released cytokines/chemokines among the two cell populations studied. These findings establish an important role for IL‐16 in modulating the activity of APC and may have relevance regarding the protection of reservoir cells against HIV‐1 infection.