Suggestions(2)
Exact(4)
Consequently, differences in other surface structures, such as O. anthropi lipoproteins or extracellular polysaccharides [51], should be responsible for complement activation and the ensuing proinflammatory activities.
Since LPS is one of the main molecules responsible for complement activation by Gram negative cell surfaces, we tested whether the O. anthropi LPS (OaLPS) consumed complement.
Ixoderins are tick lectins related to ficolins, which are responsible for complement activation, and to arthropod lectins, which act as plasma agglutination activators.
As the C-terminal globular domain of COMP, which is the domain responsible for complement activation [ 26], is engaged in multiple interactions in tissues, it is also possible that COMP needs to detach from its interacting partners in the tissue for it to be able to stimulate complement.
Similar(56)
Secondly, GD2-specific CARs lack the antibody Fc domain that is considered responsible for complement-dependent toxicities, including the neuropathic pain syndrome (Sorkin et al, 2010).
Poloxamer addition to plasma/serum (at levels above its critical micelle concentration, cmc) induced formation of large and diffused structures, which may have been responsible for triggering complement.
Therefore, other O. anthropi surface molecules, such as capsule polysaccharides, may be responsible for binding complement.
C-reactive protein (CRP) is an acute phase protein in humans and it was reported to be (in part) responsible for the complement activation in AMI [10] [12].
Blocking CR3-HIV-1 binding decreased MHCI presentation by IDCs and MDCs of F-HIV (27.4%, p = 0.083: 18.2%, p = 0.19) and C-HIV (25.5%, p = 0.03: 43.5%, p = 0.0003) (Fig. 2A and B), indicating that CR3 was responsible for guiding complement-opsonized virions to MHCI presentation.
In the absence of specific antibodies, the complement alternative and lectin pathways are responsible for triggering the complement system against the pathogens in the bloodstream.
The lack of proper regulation of the AP convertase may be responsible for the increased complement activation that has been observed in DHF patients (Figure 6; Table 3).
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