By their interaction with IgG immune complexes, FcR and complement link innate and adaptive immunity, showing functional redundancy. In complement-deficient mice, IgG downstream effector functions are often impaired, as well as adaptive immunity. Based on a variety of model systems using FcR-knockout mice, it has been concluded that FcRs are also key regulators of innate and adaptive immunity; however, several of the model systems underpinning these conclusions suffer from flawed experimental design. To address this issue, we generated a novel mouse model deficient for all FcRs (FcRI/II/III/IV–/– mice). These mice displayed normal development and lymphoid and myeloid ontogeny. Although IgG effector pathways were impaired, adaptive immune responses to a variety of challenges, including bacterial infection and IgG immune complexes, were not. Like FcRIIb-deficient mice, FcRI/II/III/IV–/– mice developed higher Ab titers but no autoantibodies. These observations indicate a redundant role for activating FcRs in the modulation of the adaptive immune response in vivo. We conclude that FcRs are downstream IgG effector molecules with a restricted role in the ontogeny and maintenance of the immune system, as well as the regulation of adaptive immunity.
from The Journal of Immunology current issue https://ift.tt/2qm52dl
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