Faculty Opinions recommendation of CD4+ T cell polarization in mice is modulated by strain-specific major histocompatibility complex-independent differences within dendritic cells.

Author(s):  
Torben Lund
2014 ◽  
Vol 21 (5) ◽  
pp. 641-650 ◽  
Author(s):  
Rachel M. Stenger ◽  
Hugo D. Meiring ◽  
Betsy Kuipers ◽  
Martien Poelen ◽  
Jacqueline A. M. van Gaans-van den Brink ◽  
...  

ABSTRACTKnowledge of naturally processedBordetella pertussis-specific T cell epitopes may help to increase our understanding of the basis of cell-mediated immune mechanisms to control this reemerging pathogen. Here, we elucidate for the first time the dominant major histocompatibility complex (MHC) class II-presentedB. pertussisCD4+T cell epitopes, expressed on human monocyte-derived dendritic cells (MDDC) after the processing of whole bacterial cells by use of a platform of immunoproteomics technology. Pertussis epitopes identified in the context of HLA-DR molecules were derived from two envelope proteins, i.e., putative periplasmic protein (PPP) and putative peptidoglycan-associated lipoprotein (PAL), and from two cytosolic proteins, i.e., 10-kDa chaperonin groES protein (groES) and adenylosuccinate synthetase (ASS). No epitopes were detectable from known virulence factors. CD4+T cell responsiveness in healthy adults against peptide pools representing epitope regions or full proteins confirmed the immunogenicity of PAL, PPP, groES, and ASS. Elevated lymphoproliferative activity to PPP, groES, and ASS in subjects within a year after the diagnosis of symptomatic pertussis suggested immunogenic exposure to these proteins during clinical infection. The PAL-, PPP-, groES-, and ASS-specific responses were associated with secretion of functional Th1 (tumor necrosis factor alpha [TNF-α] and gamma interferon [IFN-γ]) and Th2 (interleukin 5 [IL-5] and IL-13) cytokines. Relative paucity in the naturalB. pertussisepitope display of MDDC, not dominated by epitopes from known protective antigens, can interfere with the effectiveness of immune recognition ofB. pertussis. A more complete understanding of hallmarks inB. pertussis-specific immunity may advance the design of novel immunological assays and prevention strategies.


2011 ◽  
Vol 203 (12) ◽  
pp. 1763-1774 ◽  
Author(s):  
Amanda J. Chase ◽  
Freddy A. Medina ◽  
Jorge L. Muñoz-Jordán

2018 ◽  
Vol 200 (9) ◽  
pp. 3087-3099 ◽  
Author(s):  
Seung-Chul Choi ◽  
Zhiwei Xu ◽  
Wei Li ◽  
Hong Yang ◽  
Derry C. Roopenian ◽  
...  

1997 ◽  
Vol 186 (8) ◽  
pp. 1223-1232 ◽  
Author(s):  
Thomas Brocker

Thymic T cell development is controlled by T cell receptor (TCR)–major histocompatibility complex (MHC) interactions, whereas a further dependence of peripheral mature T cells on TCR–MHC contact has not been described so far. To study this question, CD4 T cell survival was surveyed in mice lacking MHC class II expression and in mice expressing MHC class II exclusively on dendritic cells. Since neither of these mice positively select CD4 T cells in the thymus, they were grafted with MHC class II–positive embryonic thymic tissue, which had been depleted of bone marrow derived cells. Although the thymus grafts in both hosts were repopulated with host origin thymocytes of identical phenotype and numbers, an accumulation of CD4+ T cells in peripheral lymphoid organs could only be observed in mice expressing MHC class II on dendritic cells, but not in mice that were completely MHC class II deficient. As assessed by histology, the accumulating peripheral CD4 T cells were found to be in close contact with MHC class II+ dendritic cells, suggesting that CD4 T cells need peripheral MHC class II expression for survival and that class II+ dendritic cells might play an important role for the longevity of CD4 T cells.


2012 ◽  
Vol 109 (25) ◽  
pp. 9977-9982 ◽  
Author(s):  
P. C. Cook ◽  
L. H. Jones ◽  
S. J. Jenkins ◽  
T. A. Wynn ◽  
J. E. Allen ◽  
...  

1993 ◽  
Vol 23 (9) ◽  
pp. 2078-2084 ◽  
Author(s):  
A. Lawrie Morton ◽  
Eric B. Bell ◽  
Eleanor M. Bolton ◽  
Hilary E. Marshall ◽  
Chris Roadknight ◽  
...  

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