X-ray Crystal Structure of C3d: A C3 Fragment and Ligand for Complement Receptor 2

Author:

Nagar Bhushan1,Jones Russell G.1,Diefenbach Russell J.1,Isenman David E.1,Rini James M.1

Affiliation:

1. Department of Biochemistry and Department of Molecular and Medical Genetics, University of Toronto, Toronto, Ontario, M5S 1A8, Canada.

Abstract

Activation and covalent attachment of complement component C3 to pathogens is the key step in complement-mediated host defense. Additionally, the antigen-bound C3d fragment interacts with complement receptor 2 (CR2; also known as CD21) on B cells and thereby contributes to the initiation of an acquired humoral response. The x-ray crystal structure of human C3d solved at 2.0 angstroms resolution reveals an α-α barrel with the residues responsible for thioester formation and covalent attachment at one end and an acidic pocket at the other. The structure supports a model whereby the transition of native C3 to its functionally active state involves the disruption of a complementary domain interface and provides insight into the basis for the interaction between C3d and CR2.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference37 articles.

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4. C3d of Complement as a Molecular Adjuvant: Bridging Innate and Acquired Immunity

5. Expression and purification were done as follows. A human C3d cDNA corresponding to residues 996 through 1303 containing the Cys 1010 → A 1010 mutation (14) was inserted into the bacterial expression plasmid pET 15b (Novogen) in which the NH 2 -terminal oligo-His encoding sequence has been deleted. The encoded C3d fragment contained an additional eight amino acids (MLDAERLK) (21) at the NH 2 -terminus that would not be present in enzymatically produced C3d ML being vector derived and DAERLK corresponding to residues at the COOH-terminus of C3g. Protein expression in transformed E. coli strain BL21 (DE3) grown in Luria Bertoni broth with ampicillin was induced with 0.25 mM isopropyl-β- d -thiogalactopyranoside (IPTG) at 28°C for 12 hours. Selenomethionine (SeMet) C3d was expressed in the same cells grown in ampicillin-containing M9 minimal medium supplemented with 0.4% glucose MgSO 4 (100 mg/ml) CaCl 2 (15 mg/ml) and thiamine (1.25 mg/ml). After IPTG induction the medium was further supplemented with the amino acids K L I V T and F (100 mg/ml each) and seleno- l -methionine (50 mg/ml) (22). Both native C3d and the SeMet C3d were purified from the soluble fraction of the bacterial lysate by DEAE-Sephacel then by Mono Q HR10/10 fast protein liquid chromatography (FPLC) (Pharmacia) both at pH 7.1 and finally by Mono S HR5/5 FPLC (Pharmacia) at pH 6. Amino acid composition analysis of SeMet C3d showed that the replacement of the eight Met positions by SeMet was near quantitative. Recombinant C3d Cys 1010 → Ala 1010 was assessed for binding to human Raji B cell–associated CR2 with a rosette inhibition assay (17). Serum-derived C3dg was used as a positive control. As monomeric ligands both proteins inhibited 50% of rosette formation at 0.2 μM.

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