Although ANCAs were found in the majority of animals, the massive presence of glomerular immune deposits differed from the pauci-immune pattern found in human AASV, making this model not completely representative for human ANCA-associated CGN. However, the spontaneous and concomitant development of pANCA, small vessel vasculitis, and CGN raises the opportunity to analyze pathogenetic links between these disease manifestations in vivo.
Deoxyspergualin achieved a high rate of disease remission and permitted prednisolone reduction in refractory or relapsing Wegener's granulomatosis. Adverse events were common but rarely led to treatment discontinuation.
The effect of deoxyspergualin (DSG, NKT-01) on humoral immunity was investigated both in vitro and in vivo. DSGinhibited the primary and secondary responses to T cell-dependent antigens and the response to T cell-independent antigens in thymic and athymic mice. However, natural antibodies in non-sensitized mice were affected less by the administration ofDSG. The agent produced a dose-dependent inhibition of B cell proliferation and antibody production to lipopolysaccharide in vitro. Suppression of secondary antibody response was also shown, whenever antigen stimulation was not given, antibody production was not affected. These results suggest that DSGaffects the proliferative stage ofB lymphocytes in such a way as to inhibit their growth and antibody production.
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