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. 2021 Apr 29;12:662164. doi: 10.3389/fimmu.2021.662164

Table 3.

Pathogen evasion.

Ligand Site on CR3 Site on ligand Function
Staphylococcus aureus
Leukocidin GH
αMI (MIDAS) LukH (main) & LukG Pore formation, virulence (41, 42)
Streptococcus pneumoniae - Pneumolysin sLex on αMI Pore formation (123)
Mycobacterium tuberculosis and smegmatis αMI (not iC3b site), C-terminal for M. tuberculosis, competes with laminarin and NADG Binding and internalization of M. tuberculosis (124)
Neisseria gonorrhoeae Activated αMI, lectin domain, cooperative with FH Pilus glycan Host evasion: internalization without inflammation (85, 125, 126)
Group B Streptococci Phagocytosis (127)
Porphyromonas gingivalis - Fimbrillin IL-12 regulation, pathogenicity (128, 129)
Bordetella pertussis Binding of CyaA Ca2+ dependent, not Mg2+ dependent, → binding is αMI-domain independent? Reduced expression of IL-12, macrophage adhesion (130134)
Bacillus anthracis - BclA Spore uptake (135)
Streptococcus pneumoniae - RrgA αMI Increased phagocytosis, virulence (136)
Franciscellas tularensis C3 opsonized results in limited inflammasome priming and pro-inflammatory cytokine production (137)
Borrelia burgdorferi – OspA, OspB Not overlapping to iC3b (138)
Leishmania sp. - gp63 Residues 365-386, 252-255 (139141)
HIV-1 (142, 143)
Herpes simplex 2 Opsonized with iC3b and without Opsonized HSV2 increased infection of DC (144)
Hantavirus In competition to heparin Increased virulence by NETosis causing severe renal and pulmonary pathology (145)
Candida albicans Competed by vitronectin, fibrinogen (αMI-domain) and NADG, β-glucan (lectin) beta-glucan candida killing by co-ligation with FH (146, 147)
Blastomyces dermatitis Via same binding site like LPS, divalent cation dependent probably via the WI-1 surface protein Increased phagocytosis, virulence (148)
Histoplasma capsulatum Divalent cation dependent, not via lectin binding site Increased phagocytosis, virulence, induction of ROS (149)