Advanced

Immune evasion by acquisition of complement inhibitors: The mould Aspergillus binds both factor H and C4b binding protein

Vogl, G; Lesiak, I; Jensen, D.B.; Perkhofer, S; Eck, R; Speth, C; Lass-Flörl, C; Zipfel, P.F.; Blom, Anna LU and Dierich, M.P., et al. (2008) In Molecular Immunology 45(5). p.1485-1493
Abstract
Pathogenic fungi represent a major threat particularly to immunocompromised hosts, leading to severe, and often lethal, systemic opportunistic infections. Although the impaired immune status of the host is clearly the most important factor leading to disease, virulence factors of the fungus also play a role. Factor H (FH) and its splice product FHL-1 represent the major fluid phase inhibitors of the alternative pathway of complement, whereas C4b-binding protein (C4bp) is the main fluid phase inhibitor of the classical and lectin pathways. Both proteins can bind to the surface of various human pathogens conveying resistance to complement destruction and thus contribute to their pathogenic potential. We have recently shown that Candida... (More)
Pathogenic fungi represent a major threat particularly to immunocompromised hosts, leading to severe, and often lethal, systemic opportunistic infections. Although the impaired immune status of the host is clearly the most important factor leading to disease, virulence factors of the fungus also play a role. Factor H (FH) and its splice product FHL-1 represent the major fluid phase inhibitors of the alternative pathway of complement, whereas C4b-binding protein (C4bp) is the main fluid phase inhibitor of the classical and lectin pathways. Both proteins can bind to the surface of various human pathogens conveying resistance to complement destruction and thus contribute to their pathogenic potential. We have recently shown that Candida albicans evades complement by binding both Factor H and C4bp. Here we show that moulds such as Aspergillus spp. bind Factor H, the splicing variant FHL-1 and also C4bp. Immunofluorescence and flow cytometry studies show that the binding of Factor H and C4bp to Aspergillus spp. appears to be even stronger than to Candida spp. and that different, albeit possibly nearby, binding moieties mediate this surface attachment. (Less)
Please use this url to cite or link to this publication:
author
, et al. (More)
(Less)
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Evasion, Aspergillus spp., Candida spp., Factor H (FH), C4b binding protein (C4bp)
in
Molecular Immunology
volume
45
issue
5
pages
1485 - 1493
publisher
Pergamon
external identifiers
  • pmid:17915330
  • wos:000253030000031
  • scopus:37349060281
ISSN
1872-9142
DOI
10.1016/j.molimm.2007.08.011
language
English
LU publication?
yes
id
8389c7bd-20e1-4623-8f82-a3e92f55c8d8 (old id 1138706)
date added to LUP
2008-04-29 09:23:28
date last changed
2017-04-16 03:43:12
@article{8389c7bd-20e1-4623-8f82-a3e92f55c8d8,
  abstract     = {Pathogenic fungi represent a major threat particularly to immunocompromised hosts, leading to severe, and often lethal, systemic opportunistic infections. Although the impaired immune status of the host is clearly the most important factor leading to disease, virulence factors of the fungus also play a role. Factor H (FH) and its splice product FHL-1 represent the major fluid phase inhibitors of the alternative pathway of complement, whereas C4b-binding protein (C4bp) is the main fluid phase inhibitor of the classical and lectin pathways. Both proteins can bind to the surface of various human pathogens conveying resistance to complement destruction and thus contribute to their pathogenic potential. We have recently shown that Candida albicans evades complement by binding both Factor H and C4bp. Here we show that moulds such as Aspergillus spp. bind Factor H, the splicing variant FHL-1 and also C4bp. Immunofluorescence and flow cytometry studies show that the binding of Factor H and C4bp to Aspergillus spp. appears to be even stronger than to Candida spp. and that different, albeit possibly nearby, binding moieties mediate this surface attachment.},
  author       = {Vogl, G and Lesiak, I and Jensen, D.B. and Perkhofer, S and Eck, R and Speth, C and Lass-Flörl, C and Zipfel, P.F. and Blom, Anna and Dierich, M.P. and Würzner, R.},
  issn         = {1872-9142},
  keyword      = {Evasion,Aspergillus spp.,Candida spp.,Factor H (FH),C4b binding protein (C4bp)},
  language     = {eng},
  number       = {5},
  pages        = {1485--1493},
  publisher    = {Pergamon},
  series       = {Molecular Immunology},
  title        = {Immune evasion by acquisition of complement inhibitors: The mould Aspergillus binds both factor H and C4b binding protein},
  url          = {http://dx.doi.org/10.1016/j.molimm.2007.08.011},
  volume       = {45},
  year         = {2008},
}