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. 1999 Aug 2;190(3):331–340. doi: 10.1084/jem.190.3.331

Table 4.

Recognition by Opa Variants of Mutant Full-length CD66b Receptors Expressed by CHO Cells

Transfectant Recognition by Opa variants
OpaB OpaC OpaI
CD66b
R29F +/− +/−
N32S + +
A41G +/− +/−
R44Q
N32S+R29F ++ + ++
N32S+A41G ++ + ++
N32S+R44Q + +
RF29F+N32S+A41G ++/fp ++ ++/fp
CD66e/b ++/fp ++ ++/fp
CD66e ++/fp ++ ++/fp

Interaction with Opa variants was determined by evaluating the percentage of receptor-positive cells that had significant amounts of associated gonococci (>5 bacteria per cell). Presence of receptor and bacteria was determined by immunofluorescence microscopy. The first column indicates the mutations made in CD66b; CD66e/b and CD66e indicate that the entire CD66b N-domain was replaced with either the chimeric N-domain mentioned in Table or the entire native CD66e N-domain. The results were tabulated as follows: ++/fp, all receptor-positive cells were infected plus numerous footprints were present; ++, 60–90% of receptor-positive cells were infected; +, 30–60% of receptor-positive cells were infected; +/−, 10–30% of receptor-positive cells were infected; −, no infected cells present. Infection experiments with recombinant MS11 Opa variants (reference 5) resulted in identical recognition patterns as those shown here for wild-type MS11 Opa variants. Results represent the mean of two to four independent experiments.