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Abstract: We will not speak here of type III hypersensitivity reactions (the Arthus reaction), in which immune complexes of antigen and antibody react with FcγR receptors on polymorphonuclear leukocytes and, after activating complement, attract cells via chemotactic anaphylatoxins such as C5a (1,2). Rather, we are interested in the role that polymorphonuclear leukocytes play in hypersensitivity reactions where, until recently, only eosinophils, among the granulocytes, appeared to be involved. [Copyright &y& Elsevier]

The high frequency of meningococcal infections in patients with congenital deficiency of a component of the complement terminal pathway emphasizes the critical role of this system in host resistance against Neisseriaceae. We report the observation of a subacute septicaemia due to N. meningitidis serogroup Y. This girl had an acquired deficit of the C3 fraction of complement due to a high titre of C3 nephritic factor (C3NeF). There was no evidence of partial lipodystrophy or biological symptoms of glomerular disease. The meningococcal infection revealed this biological abnormality.