MS V186 DRIVER DETAILS:
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MS V186 DRIVER
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Three mice from each group were killed and examined for splenic GC and AFC on days 8 and 12 after the immunization. The athymic mice that were supplemented with helper T cells 3 days after the immunization with NP-CGG see the experimental design, Table 1group I control demonstrated a slow and diminished anti-NP ms v186 as expected. Serum anti-NP antibody of IgM, IgG1 and IgG3 isotypes became detectable by the 2nd week after the immunization and their titres, particularly for the IgG isotypes, were 1—2 log lower than those in the normal R, reference response group Fig.
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Likewise, there were no GC detectable in the spleens of these ms v186 until day 12 after the immunization Fig. The serum levels of passive IgG1 in these experimental mice mimicked the levels of actively produced anti-NP IgG1 in normal animals Fig.
Thus, ms v186 is apparent that passive administration of IgG1 antibody produced a dramatic effect on the GC formation without affecting the serum levels of endogenous antibodies of other isotypes. It should be noted that the stimulation of GC response by passive IgG1 antibody was T-cell-dependent. V H gene repertoire of transformed colonies with VDJ segments recovered from the germinal centres and from the foci of antibody-forming cells.
Interestingly, the V H gene repertoire shift in mice with passive IgG1 antibody appeared to be restricted to the GC developmental pathway because it did not occur among the AFC. We screened the V H gene usage in NP-binding plasmacytes within the antibody foci in the same spleens and found little effect of passive IgG1 on their clonotypic repertoire Table ms v186.
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