IrC2/Bf - A yeast and Borrelia responsive component of the complement system from the hard tick Ixodes ricinus
Language English Country United States Media print-electronic
Document type Journal Article
PubMed
29061482
DOI
10.1016/j.dci.2017.10.012
PII: S0145-305X(17)30475-5
Knihovny.cz E-resources
- Keywords
- Borrelia, C3-complement convertase, Factor B, Ixodes, Phagocytosis, Tick immunity,
- MeSH
- Complement Activation MeSH
- Borrelia burgdorferi immunology MeSH
- Candida albicans immunology MeSH
- Phagocytosis MeSH
- Hemocytes immunology microbiology MeSH
- Insect Proteins genetics metabolism MeSH
- Disease Vectors MeSH
- Host-Pathogen Interactions MeSH
- Candidiasis immunology MeSH
- Ixodes immunology MeSH
- Complement C3 genetics metabolism MeSH
- Humans MeSH
- Lyme Disease immunology MeSH
- RNA, Small Interfering genetics MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Insect Proteins MeSH
- Complement C3 MeSH
- RNA, Small Interfering MeSH
Ticks possess components of a primordial complement system that presumably play a role in the interaction of the tick immune system with tick-borne pathogens and affect their transmission. Here we characterized a novel complement component, tagged as IrC2/Bf, from the hard tick Ixodes ricinus, the principal vector of Lyme disease in Europe. IrC2/Bf is a multi-domain molecule composed of 5-7 CCP modules, varied by alternative splicing, followed by a von Willebrand factor A domain and a C-terminal trypsin-like domain. The primary structure and molecular architecture of IrC2/Bf displays the closest homology to the C3-complement component convertases described in horseshoe crabs. The irc2/bf gene is mainly expressed in the tick fat body associated with the trachea and, as determined by western blotting, the protein is present in low amounts in tick hemolymph. Expression of irc2/bf mRNA was significantly up-regulated in response to the intra-hemocoelic injection of the yeast Candida albicans and all tested Borrelia sp. strains (B. burgdorferi NE5264, B. burgdorferi CB26, B. garinii MSLB, B. afzelii CB43), but was not affected by injection of model Gram-negative and Gram-positive bacteria or the aseptic injection control. In-line with these results, RNAi-mediated silencing of irc2/bf inhibited phagocytosis of B. afzelii and C. albicans but not the other bacteria. Tissue expression profiles, specific responses to microbial challenges, and patterns of phagocytic phenotypes upon RNAi silencing observed for IrC2/Bf match well with the previously reported characteristics of I. ricinus C3-related molecule 1 (IrC3-1). Therefore we presume that IrC2/Bf functions as a convertase in the same complement activation pathway protecting ticks against yeast and Borrelia infection.
References provided by Crossref.org
Tick Immune System: What Is Known, the Interconnections, the Gaps, and the Challenges
Tracking of Borrelia afzelii Transmission from Infected Ixodes ricinus Nymphs to Mice