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To counteract this, pathogen effectors target and inhibit individual PTI steps. It involves pattern-triggered immunity (PTI), which is signaled and manifested through branched multi-step pathways. Knowledge of the binding site has resulted in engineering efforts to modulate IgG effector functions – see Fc engineering section for more detail.The immune system of plants is highly complex. Effector FunctionĪs shown in the model below FcγRs bind to IgG asymmetrically across the hinge and upper CH2 region.

See the table below for IgG subtype variation in effector functions, ranked in decreasing potency. Although this is dependent on the allotype and specific FcvR in simple terms ADCC effector function is high for human IgG1 and IgG3, and low for IgG2 and IgG4. The level of ADCC effector function various for IgG subtypes. Upon binding a signalling pathway is triggered which results in the secretion of various substances, such as lytic enzymes, perforin, granzymes and tumour necrosis factor, which mediate in the destruction of the target cell. In antibody dependent cellular cytotoxicity (ADCC), FcvRs on the surface of effector cells (natural killer cells, macrophages, monocytes and eosinophils) bind to the Fc region of an IgG which itself is bound to a target cell. FcγRI is classed as a high affinity receptor (nanomolar range KD) while FcγRII and FcγRIII are low to intermediate affinity (micromolar range KD) (1). There are three classes of receptors for human IgG found on leukocytes: CD64 (FcγRI), CD32 (FcγRIIa, FcγRIIb and FcγRIIc) and CD16 (FcγRIIIa and FcγRIIIb). Receptors for all classes of immunoglobulins have been identified, including FcγR (IgG), FcεRI (IgE), FcαRI (IgA), FcμR (IgM) and FcδR (IgD).