Decay accelerating factor (DAF) as the host antigen with protective activity to complement killing of schistosomula

Fj, Ramalho-Pinto

doi:10.1590/s0074-02761987000800037

Cited by 11 publications

(5 citation statements)

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“…Resistance appears in part secondary to the presence of an innate trypsin-sensitive, membrane-bound regulatory protein that is distinct from DAF and CR1. Moreover, these organisms appear able to pirate DAF molecules from host cells for their own protection (267,268,282).…”

Section: Microbial Interactions With Complementmentioning

confidence: 99%

Infectious diseases associated with complement deficiencies

1991

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The complement system consists of both plasma and membrane proteins. The former influence the inflammatory response, immune modulation, and host defense. The latter are complement receptors, which mediate the cellular effects of complement activation, and regulatory proteins, which protect host cells from complement-mediated injury. Complement activation occurs via either the classical or the alternative pathway, which converge at the level of C3 and share a sequence of terminal components. Four aspects of the complement cascade are critical to its function and regulation: (i) activation of the classical pathway, (ii) activation of the alternative pathway, (iii) C3 convertase formation and C3 deposition, and (iv) membrane attack complex assembly and insertion. In general, mechanisms evolved by pathogenic microbes to resist the effects of complement are targeted to these four steps. Because individual complement proteins subserve unique functional activities and are activated in a sequential manner, complement deficiency states are associated with predictable defects in complement-dependent functions. These deficiency states can be grouped by which of the above four mechanisms they disrupt. They are distinguished by unique epidemiologic, clinical, and microbiologic features and are most prevalent in patients with certain rheumatologic and infectious diseases. Ethnic background and the incidence of infection are important cofactors determining this prevalence. Although complement undoubtedly plays a role in host defense against many microbial pathogens, it appears most important in protection against encapsulated bacteria, especially Neisseria meningitidis but also Streptococcus pneumoniae, Haemophilus influenzae, and, to a lesser extent, Neisseria gonorrhoeae. The availability of effective polysaccharide vaccines and antibiotics provides an immunologic and chemotherapeutic rationale for preventing and treating infection in patients with these deficiencies.

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Section: Microbial Interactions With Complementmentioning

confidence: 99%

Infectious diseases associated with complement deficiencies

1991

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“…An association between host-derived molecules and worms of the trematode Schistosoma mansoni has already often been demonstrated. The former include blood group (Smithers et al 1969), Forssman (Dean and Sell, 1972) and major histocompatibility complex antigens (MHC : Gitter et al 1982 ;Simpson et al 1983), immunoglobulins (Kemp et al 1977), complement decay-accelerating factor (Ramalho-Pinto, 1987), host lipids (Furlong et al 1992), lipoproteins (Dinguirard and Yoshino, 2006), and the protease inhibitors alpha-2 macroglobulin (Damian et al 1973) and contrapsin (Modha et al 1988). Doenhoff et al (1988) used immunochemistry and zymography to assay the peptidases present in different life-cycle stages of S. mansoni and found an enzyme which could hydrolyse N-acetyl-DLphenylalanine b-naphthyl ester (NAPBNE) in extracts of adult worms.…”

Section: Introductionmentioning

confidence: 99%

An association betweenSchistosoma mansoniworms and an enzymatically-active protease/peptidase in mouse blood

Darani

Doenhoff

2008

Parasitology

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An enzyme found previously in extracts of adult Schistosoma mansoni worms, that hydrolysed the chromogenic substrate N-acetyl-DL-phenylalanine beta-naphthyl-ester, has here been further investigated and characterized. Evidence that the molecule found in the parasite was antigenically and enzymatically homologous with a constituent of normal mouse plasma has been consolidated using a monospecific serum in immunoelectrophoresis and Western immunoblotting. The molecular size of the enzyme was found to be approximately 70 kDa and it was inhibited by a serine protease inhibitor, but not by inhibitors of other classes of protease. The enzymatic activity found in normal mouse serum was also found in normal rat serum, but not in sera from several other mammalian species.

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“…Some helminths have also developed strategies to avoid complement recognition in the early stages of infection. Soon after entry into the host, Schistosoma mansoni becomes resistant to serum-dependent killing by shedding a strongly antigenic coat, acquiring host proteins, including blood group antigens and the complement regulatory protein decay accelerating factor (39,41), and secreting proteins that bind to and inhibit complement proteins (13,30,32). In the early stages of infection, parasitic nematodes may also undergo changes that inhibit C3 deposition (35) and reduce the capacity of leukocytes to attach (1,5).…”

mentioning

confidence: 99%

Loss of Complement Activation and Leukocyte Adherence asNippostrongylus brasiliensisDevelops within the Murine Host

et al. 2005

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Complement activation and C3 deposition on the surface of parasitic helminths may be important for recruitment of leukocytes and for damage to the target organism via cell-mediated mechanisms. Inhibition of complement activation would therefore be advantageous to parasites, minimizing damage and enhancing migration through tissues. The aim of this study was to determine ex vivo if complement activation by, and leukocyte adherence to, the nematode Nippostrongylus brasiliensis change as the parasite matures and migrates through the murine host. Pathways of activation of complement and the mechanism of adherence of leukocytes were also defined using sera from mice genetically deficient in either C1q, factor B, C1q and factor B, C3, or C4. Substantive deposition of C3 and adherence of eosinophil-rich leukocytes were seen with infective-stage (L3) but not with lung-stage (L4) larvae. Adult intestinal worms had low to intermediate levels of both C3 and leukocyte binding. For L3 and adult worms, complement deposition was principally dependent on the alternative pathway. For lung-stage larvae, the small amount of C3 detected was dependent to similar degrees on both the lectin and alternative pathways. The classical pathway was not involved for any of the life stages of the parasite. These results suggest that in primary infections, the infective stage of N. brasiliensis is vulnerable to complement-dependent attack by leukocytes. However, within the first 24 h of infection, N. brasiliensis acquires the ability to largely avoid complement-dependent immune responses.

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Decay accelerating factor (DAF) as the host antigen with protective activity to complement killing of schistosomula

Cited by 11 publications

References 0 publications

Infectious diseases associated with complement deficiencies

Infectious diseases associated with complement deficiencies

An association betweenSchistosoma mansoniworms and an enzymatically-active protease/peptidase in mouse blood

Loss of Complement Activation and Leukocyte Adherence asNippostrongylus brasiliensisDevelops within the Murine Host

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