Rituximab is a chimeric monoclonal antibody directed against
CD20 on human B cells. In laboratory studies, rituximab binds CD20 equally well
on human B cells in both human and murine environment (eg mice transplanted with
a human B cell lymphoma). However, effective B‑cell depletion is observed only
when human complement or human Fc receptor–expressing
effector cells are present. Clinically, the degree of B‑cell
depletion correlates with intact complement activity and Fcγ receptor–mediated
effector function rather than with antibody binding alone.

Considering these observations, why is the human
constant (Fc) region functionally essential for rituximab’s therapeutic effect?

Question

Rituximab is a chimeric monoclonal antibody directed against
CD20 on human B cells. In laboratory studies, rituximab binds CD20 equally well
on human B cells in both human and murine environment (eg mice transplanted with
a human B cell lymphoma). However, effective B‑cell depletion is observed only
when human complement or human Fc receptor–expressing
effector cells are present. Clinically, the degree of B‑cell
depletion correlates with intact complement activity and Fcγ receptor–mediated
effector function rather than with antibody binding alone.

Considering these observations, why is the human
constant (Fc) region functionally essential for rituximab’s therapeutic effect?

Accepted Answer

To
enable recruitment of human immune effector mechanisms such as complement
activation and Fc receptor‑mediated cytotoxicity

Answer

To
extend serum half‑life through enhanced neonatal Fc receptor
recycling

Answer

To
reduce immunogenicity and prevent the formation of anti‑drug antibodies

Answer

To
standardise dosing behaviour across monoclonal antibody therapies

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