Mice homozygous for the C4 (complement component C4) targeted mutation are viable and fertile. Homozygous mutants exhibit an increased susceptibility to lethal infection by Group B streptococci(GBS). C4 homozygous mutants show a similar susceptibility to GBS lethal infection as do C3 null mice, suggesting that the classical, and not alternative, pathway is primarily involved in antibody-independent humoral immunity to GBS. Homozygotes also demonstrate a profound defect in antibody response to T cell dependent antigens. They show a diminished level of peanut agglutin+ germinal centers and a failure in isotype switching despite normal B cell signalling in vitro.

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These C4b knock-out mice exhibit an increased susceptibility to lethal infection by Group B streptococci.

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