Open AccessThe B subunit of Escherichia coli heat‐labile toxin alters the development and antigen‐presenting capacity of dendritic cells
Author(s) -
Ji Jing,
Griffiths Kristin L,
Milburn Peter J,
Hirst Timothy R,
O'Neill Helen C
Publication year - 2015
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12599
Subject(s) - heat labile enterotoxin , antigen , dendritic cell , population , t cell , spleen , adjuvant , biology , immunology , chemistry , microbiology and biotechnology , enterotoxin , immune system , biochemistry , escherichia coli , medicine , environmental health , gene
Escherichia coli 's heat‐labile enterotoxin (Etx) and its non‐toxic B subunit (EtxB) have been characterized as adjuvants capable of enhancing T cell responses to co‐administered antigen. Here, we investigate the direct effect of intravenously administered EtxB on the size of the dendritic and myeloid cell populations in spleen. EtxB treatment appears to enhance the development and turnover of dendritic and myeloid cells from precursors within the spleen. EtxB treatment also gives a dendritic cell ( DC ) population with higher viability and lower activation status based on the reduced expression of MHC ‐II, CD 80 and CD 86. In this respect, the in vivo effect of EtxB differs from that of the highly inflammatory mediator lipopolysaccharide. In in vitro bone marrow cultures, EtxB treatment was also found to enhance the development of DC from precursors dependent on Flt3L. In terms of the in vivo effect of EtxB on CD 4 and CD 8 T cell responses in mice, the interaction of EtxB directly with DC was demonstrated following conditional depletion of CD 11c + DC . In summary, all results are consistent with EtxB displaying adjuvant ability by enhancing the turnover of DC in spleen, leading to newly mature myeloid and DC in spleen, thereby increasing DC capacity to perform as antigen‐presenting cells on encounter with T cells.