Low-affinity (F/F and F/V) polymorphisms of FcγRIIIa (CD16) are thought to predict lower response rates and shorter duration of responses to rituximab.
The Relationship of FcRIIIa Genotype to Degree of B Cell Depletion by Rituximab in the Treatment of Systemic Lupus Erythematosus
From the article:
The Relationship of FcRIIIa Genotype to Degree of B Cell Depletion by Rituximab in the Treatment of Systemic Lupus Erythematosus
From the article:
For example, if FcRIIIa on effector cells plays an important
role in the depletion of B cells by rituximab, then patients who are homozygous or heterozygous for the high-affinity V allele (which has a 10-fold higher affinity for IgG1, the isotype of the humanized Fc portion of rituximab) should deplete B cells to a greater extent than those who are homozygous for the low-affinity F allele, at any given rituximab level. This is depicted in Figure 2, where the percentage of B cells is plotted as a function of the rituximab level for the low-affinity (FF; n 5) versus the high-affinity (VV or VF; n 7) cohorts.
As predicted, patients with the low-affinity FF genotype required about a 10-fold increase in rituximab levels to achieve the same degree of B cell depletion as that in patients with the high-affinity genotypes (VV or VF) (Figure 2).
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