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Titolo:
Mechanism of complement resistance of pathogenic Borrelia burgdorferi isolates
Autore:
Kraiczy, P; Skerka, C; Kirschfink, M; Zipfel, PF; Brade, V;
Indirizzi:
Univ Hosp Frankfurt, Inst Med Microbiol, D-60596 Frankfurt, Germany Univ Hosp Frankfurt Frankfurt Germany D-60596 D-60596 Frankfurt, Germany Hans Knoell Inst Nat Prod Res, Dept Infect Biol, Jena, Germany Hans KnoellInst Nat Prod Res Jena Germany t Infect Biol, Jena, Germany Univ Heidelberg, Dept Immunol, Heidelberg, Germany Univ Heidelberg Heidelberg Germany g, Dept Immunol, Heidelberg, Germany
Titolo Testata:
INTERNATIONAL IMMUNOPHARMACOLOGY
fascicolo: 3, volume: 1, anno: 2001,
pagine: 393 - 401
SICI:
1567-5769(200103)1:3<393:MOCROP>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN FACTOR-H; STREPTOCOCCAL-M-PROTEINS; LYME-DISEASE SPIROCHETE; SERUM RESISTANCE; NEISSERIA-GONORRHOEAE; BURGDORFERI STRAINS; ALTERNATIVE PATHWAY; REGULATORY DOMAINS; MEMBRANE-PROTEINS; IMMUNOGLOBULIN-G;
Keywords:
Borrelia burgdorferi; Lyme disease; complement; innate immunity; immune evasion; factor H; FHL-1/reconectin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
55
Recensione:
Indirizzi per estratti:
Indirizzo: Kraiczy, P Univ Hosp Frankfurt, Inst Med Microbiol, Paul Ehrlich Str 40, D-60596 Frankfurt, Germany Univ Hosp Frankfurt Paul Ehrlich Str 40 Frankfurt Germany D-60596
Citazione:
P. Kraiczy et al., "Mechanism of complement resistance of pathogenic Borrelia burgdorferi isolates", INT IMMUNO, 1(3), 2001, pp. 393-401

Abstract

Borrelia burgdorferi. the causative agent of Lyme disease. differ in theirsusceptibility to normal human serum and are consequently classified as complement-resistant. complement-sensitive and intermediate complement-sensitive. Most isolates belonging to the genospecies B. afzelii are complement-resistant. while particularly B, garinii isolates were rapidly killed by complement. In general, isolates of the genospecies B. burgdorferi sensu stricto (s.s.) are intermediate complement-sensitive. Independent of the genospecies, all Borreliae were capable to activate the classical and/or the alternative pathway. Deposition of the activation products C3, C6, and TCC is much stronger by B. burgdorferi s.s, and B. garinii isolates than by B. afzelii isolates. The mechanism(s) on how Borreliae evade complement-mediated bacteriolysis has recently been described by showing that complement-resistant B. afzelii isolates but not the complement-sensitive B. garinii isolates absorb human complement regulators FHL-1/reconectin and factor H. Surface-attached FHL-1/reconectin maintains its complement regulatory activity and supports factor I-mediated C3b cleavage to iC3b. In complement-resistant Borreliae. two outer surface proteins, the 27.5 kDa (CRASP-1, complement regulator-acquiring surface protein 1) and the 10/21 kDa (CRASP-2), are responsible for the surface attachment of the two complement regulators. GRASP-1. which is present in complement-resistant Borreliae, binds preferentially FHL-1/reconectin while GRASP-1, which is restrictively expressed, binds preferentially factor H. Thus, complement-resistant Borreliae bind human complement regulators and control complement activation on their surface and prevent the formation of toxic activation products. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 08:29:09