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. 2018 Sep 24;9:2050. doi: 10.3389/fimmu.2018.02050

Figure 2.

Figure 2

Speculated T-cell and B-cell responses following complement activation after trauma. Activation and dysregulation of complement factors and receptors following trauma may modulate key pathways in T-cells and B-cells. Trauma associated generation of activated complement products have been depicted with dotted lines. All these pathways are discussed in text and are potential areas where trauma research can focus upon. Apaf-1, Apoptotic protease activating factor 1; ATP, adenosine triphosphate; BCR, B-cell receptor; BLNK1/SLP-65, B cell linker protein 1; CD, cluster of differentiation; DNA, deoxyribonucleic acid; FAS: Fas cell surface death receptor; GATA3, GATA3 binding protein; Glut1, Glucose transporter 1; IFN-I, type-I interferon; IL, interleukin; IP3, inositol trisphosphate; ITAMs, immunoreceptor tyrosine-based activation motifs; LAMTOR, lysosomal adaptor and mitogen-activated protein kinase and mammalian target of rapamycin [mTOR] activator/regulator; LAT1, L-type amino acid transporter 1; Lck, Tyrosine-protein kinase Lck; MAC, membrane attack complex; NAD, nicotinamide adenine dinucleotide; PARP, poly (ADP-ribose) polymerase; PI3K, phosphoinositide 3-kinase; PLC-ɤ, phospholipase C- ɤ; Src, Proto-oncogene tyrosine-protein kinase Src; Syk, spleen tyrosine kinase; Th, T helper; VaV, Proto-oncogene vav; ZAP-70, Zeta-chain-associated protein kinase 70.