Activated CD8+ T lymphocytes induce differentiation of monocytes to dendritic cells and restore the stimulatory capacity of interleukin 10-treated antigen-presenting cells.
We analyzed the role of CD8+ T cells on dendritic cells (DCs). Incubation of monocytes with activated but not resting CD8+ T cells induced their differentiation into DCs with a CD1a+ and CD14- phenotype. Activated CD8+ lymphocytes induced down-regulation of CD14 expression in interleukin (IL)-10-treated macrophages and resulted in the expression of DC-related CD1a and up-regulation of mRNA transcripts for RelB, IL-12p40, MCP-2, MIP-1alpha, and ELC. These DCs were potent stimulatory cells in mixed lymphocyte reaction and induced primary CTL responses. This interaction was independent of a direct cell-to-cell contact. Monoclonal antibodies against IFN-gamma completely abolished the CD1a induction on IL-10-treated antigen-presenting cells. These results demonstrate that CD8+ cells can provide stimulatory signals to antigen-presenting cells to induce their differentiation in DC and to increase their immunostimulatory capacity.
University of Tübingen, Department of Hematology, Oncology and Immunology, D-72076 Tübingen, Germany.
Stefan
S
Wirths
Jeannette
J
Reichert
Frank
F
Grünebach
Peter
P
Brossart
D000938:Antigen-Presenting Cells / Q000187:drug effects / Q000276:immunology* / Q000502:physiology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D002450:Cell Communication / Q000276:immunology*; D002454:Cell Differentiation / Q000276:immunology; D018925:Chemokines / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D003713:Dendritic Cells / Q000166:cytology / Q000276:immunology*; D015536:Down-Regulation / Q000276:immunology; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D007371:Interferon-gamma / Q000276:immunology; D016753:Interleukin-10 / Q000276:immunology / Q000494:pharmacology*; D018664:Interleukin-12 / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D053762:Interleukin-12 Subunit p40; D018950:Lipopolysaccharide Receptors / Q000276:immunology / Q000378:metabolism; D008213:Lymphocyte Activation / Q000276:immunology; D008264:Macrophages / Q000166:cytology / Q000187:drug effects / Q000276:immunology; D009000:Monocytes / Q000166:cytology / Q000276:immunology*; D021122:Protein Subunits; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D051841:Transcription Factor RelB; D014157:Transcription Factors / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D015854:Up-Regulation / Q000276:immunology
D018925:Chemokines; D053762:Interleukin-12 Subunit p40; D018950:Lipopolysaccharide Receptors; D021122:Protein Subunits; D011518:Proto-Oncogene Proteins; C497593:RELB protein, human; D014157:Transcription Factors; D016753:Interleukin-10; D051841:Transcription Factor RelB; D018664:Interleukin-12; D007371:Interferon-gamma