Mycoplasma pneumoniae infection in the human is often followed by a transient autoimmune hemolytic disorder characterized by high titer autoantibodies to a carbohydrate antigen, the I antigen. Because the major host cell receptor for the Mycoplasma is the sialylated form of this antigen, it is likely that the immunologic disorder is initiated by the microbe-saccharide interaction. Here we review briefly knowledge on the autoantibodies and the structures and distribution of the saccharide antigens and receptors. We discuss possible mechanisms for the triggering of autoantibody production and consider ways in which perturbation of various glycoprotein carriers of the carbohydrate ligands may elicit a variety of pathobiologic responses. We conclude by highlighting ideas on further molecular dissections of the elements of the microbe-host interaction.