The Elements Steering Pathogenesis in IgG-Mediated Alloimmune Diseases.
Myrthe E SonneveldC Ellen van der SchootGestur VidarssonPublished in: Journal of clinical immunology (2016)
Alloimmune diseases can occur in pregnancy and after blood transfusions, where antibodies are formed, targeting foreign cells and tissues for destruction by myeloid cells through IgG Fc-receptors (FcγR). In pregnancy, antibodies against human blood group or platelet antigens (e.g. HPA1-a) cause life-threatening anemia or thrombocytopenia in the developing fetus or newborn. Here we discuss how both the induction of those IgG antibodies as well as the proinflammatory status of the fetus affects the effector functions through FcγR. Recent studies have found IgG-glycosylation to be important with low IgG-Fc-core fucosylation resulting in increased affinity to FcγRIIIa and FcγRIIIb and enhanced antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis. The importance of these and other features, including oxidative stress and acute phase responses (C-reactive protein, CRP), will be discussed and how these features may collectively synergize resulting in elevated disease pathology in these allo-, but also autoimmune mediated diseases.
Keyphrases
- induced apoptosis
- oxidative stress
- cell cycle arrest
- dendritic cells
- endothelial cells
- endoplasmic reticulum stress
- preterm birth
- gene expression
- multiple sclerosis
- dna damage
- chronic kidney disease
- acute myeloid leukemia
- cell death
- signaling pathway
- ischemia reperfusion injury
- immune response
- pi k akt
- cancer therapy
- induced pluripotent stem cells
- diabetic rats
- drug induced
- capillary electrophoresis