4M76

Integrin I domain of complement receptor 3 in complex with C3d

Summary for 4M76

• Entry DOI: 10.2210/pdb4m76/pdb
• Descriptor: Complement C3, Integrin alpha-M, NICKEL (II) ION, ... (4 entities in total)
• Functional Keywords: integrin, complement receptor, immunity, innate immunity, inflammation, phagocytosis, mac-1, cd11b/cd18, alphambeta2, macrophage, rossmann fold, i domain, von willebrand factor a (vwa), alpha-alpha barrel, adhesion, cell adhesion
• Biological source: Homo sapiens (human); More
• Cellular location: Secreted: P01024; Membrane; Single-pass type I membrane protein: P11215
• Total number of polymer chains: 2
• Total formula weight: 55796.98

Authors

Bajic, G.,Yatime, L.,Vorup-Jensen, T.,Andersen, G.R. (deposition date: 2013-08-12, release date: 2013-10-02, Last modification date: 2024-10-09)

Primary citation

Bajic, G.,Yatime, L.,Sim, R.B.,Vorup-Jensen, T.,Andersen, G.R.
Structural insight on the recognition of surface-bound opsonins by the integrin I domain of complement receptor 3.
Proc.Natl.Acad.Sci.USA, 110:16426-16431, 2013

PubMed Abstract: Complement receptors (CRs), expressed notably on myeloid and lymphoid cells, play an essential function in the elimination of complement-opsonized pathogens and apoptotic/necrotic cells. In addition, these receptors are crucial for the cross-talk between the innate and adaptive branches of the immune system. CR3 (also known as Mac-1, integrin αMβ2, or CD11b/CD18) is expressed on all macrophages and recognizes iC3b on complement-opsonized objects, enabling their phagocytosis. We demonstrate that the C3d moiety of iC3b harbors the binding site for the CR3 αI domain, and our structure of the C3d:αI domain complex rationalizes the CR3 selectivity for iC3b. Based on extensive structural analysis, we suggest that the choice between a ligand glutamate or aspartate for coordination of a receptor metal ion-dependent adhesion site-bound metal ion is governed by the secondary structure of the ligand. Comparison of our structure to the CR2:C3d complex and the in vitro formation of a stable CR3:C3d:CR2 complex suggests a molecular mechanism for the hand-over of CR3-bound immune complexes from macrophages to CR2-presenting cells in lymph nodes.

PubMed: 24065820
DOI: 10.1073/pnas.1311261110

Experimental method

X-RAY DIFFRACTION (2.804 Å)