Parasitic helminths possess surface glycoconjugates that are recognized by the serum collectin molecule, mannose-binding lectin (MBL). Once bound, MBL triggers the lectin pathway of complement. Mice have two MBL, MBL-A and MBL-C. We previously showed that MBL-A deficient (MBL-A(-/-)) mice have enhanced survival of Brugia malayi microfilariae and abrogated microfilariae-specific IgM responses. In this study we show that MBL-A deficiency does not alter immunity to either Trichuris muris or Schistosoma mansoni. However, anti-nematode IgM levels were significantly lower in T. muris infected MBL-A(-/-) than wild-type mice. Interestingly nematode-specific IgG1 and IgG2a levels were higher in MBL-A(-/-) mice. Although, larval schistosomes are surrounded by a complement-sensitive membranous tegument, neither adult worm development, egg output, egg granuloma size nor cellular composition was affected in MBL-A(-/-) mice. In contrast to anti-nematode IgM responses, anti-schistosome IgM (and also IgG1 and IgG2b) responses were unaltered from wild-type mice. Anti-schistosome IgG2a was elevated, while IgG3 was significantly lowered, in MBL-A(-/-) mice. These results suggest that MBL-A is not a necessary component for immunity to either T. muris or S. mansoni helminths, however, MBL-A appears to be necessary for the development of specific IgM responses to nematode antigens.