Open AccessMalaria‐derived hemozoin exerts early modulatory effects on the phenotype and maturation of human dendritic cells
Author(s) -
Bujila Ioana,
Schwarzer Evelin,
Skorokhod Oleksii,
Weidner Jessica M.,
TroyeBlomberg Marita,
Östlund Farrants AnnKristin
Publication year - 2016
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12521
Subject(s) - hemozoin , biology , c c chemokine receptor type 7 , chemokine receptor , microbiology and biotechnology , chemokine , immunology , antigen presentation , immune system , dendritic cell , major histocompatibility complex , cross presentation , mhc class ii , plasmodium falciparum , homing (biology) , mhc class i , t cell , malaria , ecology
Summary Plasmodium falciparum ( P. falciparum )‐induced effects on the phenotype of human dendritic cells (DC) could contribute to poor induction of long‐lasting protective immunity against malaria. DC ability to present antigens to naïve T cells, thus initiating adaptive immune responses depends on complex switches in chemokine receptors, production of soluble mediators and expression of molecules enabling antigen‐presentation and maturation. To examine the cellular basis of these processes in the context of malaria, we performed detailed analysis of early events following exposure of human monocyte‐derived DC to natural hemozoin (nHZ) and the synthetic analog of its heme core, β‐hematin. DC exposed to either molecule produced high levels of the inflammatory chemokine MCP‐1, showed continuous high expression of the inflammatory chemokine receptor CCR5, no upregulation of the lymphoid homing receptor CCR7 and no cytoskeletal actin redistribution with loss of podosomes. DC partially matured as indicated by increased expression of major histocompatibility complex (MHC) class II and CD86 following nHZ and β‐hematin exposure, however there was a lack in expression of the maturation marker CD83 following nHZ but not β‐hematin exposure. Overall our data demonstrate that exposure to nHZ partially impairs the capacity of DC to mature, an effect in part differential to β‐hematin.