Defects in acute responses to TLR4 in Btk -deficient mice result in impaired dendritic cell-induced IFN-γ production by natural killer cells

• Published in: Clinical immunology (Orlando, Fla.) Vol. 142; no. 3; pp. 373 - 382
• Main Authors: Ní Gabhann, Joan, Spence, Shaun, Wynne, Claire, Smith, Siobhán, Byrne, Jennifer C, Coffey, Barbara, Stacey, Kevin, Kissenpfennig, Adrien, Johnston, Jim, Jefferies, Caroline A
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Inc 01.03.2012; Elsevier
• Subjects: Allergy and Immunology; Animals; Antigen presenting cells; Biological and medical sciences; Btk; Cells, Cultured; Coculture Techniques; Dendritic Cells - immunology; Fundamental and applied biological sciences. Psychology; Fundamental immunology; IFN-γ; Interferon-gamma - biosynthesis; Interferon-gamma - immunology; Killer Cells, Natural - immunology; Mice; Mice, Inbred C57BL; Natural killer cells; Protein-Tyrosine Kinases - deficiency; Protein-Tyrosine Kinases - immunology; TLRs; Toll-Like Receptor 4 - immunology; Btk; Antigen presenting cells; IFN-γ; Natural killer cells; TLRs; Dendritic cell; Toll like receptor 4; Acute; Deficiency; Rodentia; Toll like receptor; Biosynthesis; Natural killer cell; Vertebrata; Bruton tyrosine kinase; Mammalia; Immunology; Mouse; Antigen presenting cell; Animal; Gamma interferon

Abstract This study defines a critical role for Btk in regulating TLR4-induced crosstalk between antigen presenting cells (APCs) and natural killer (NK) cells. Reduced levels of IL-12, IL-18 and IFN-γ were observed in Btk -deficient mice and ex vivo generated macrophages and dendritic cells (DCs) fo...