Two classical immunological paradigms have been operated to govern the development and functionality of the antibody response: （1）affinity maturation is primarily dependent upon antigendriven selection of both the germline and somatically amended high affinity repertoires, and （2） antibody effector function is isotypically determined. Recent findings, utilizing the teleost IgM model, suggest that these classical paradigms should be broadened to incorporate the ability of the immune system to transducer the strength of antigen recognition (affinity) into isomerism structural modification that, in turn, modulate the halflife of antibody in serum. More importantly, the discovery of teleost unique feature reveals a heretofore unknown level of sophistication by which the immune system can interpret and response to the antigenic universe. The aim of this paper is to introduce key findings of recent studies in the functional explanation and cellular regulation of the affinityinduced teleost IgM isomerism, the mechanisms of longlived plasma cells, shortlived plasma cells, plasmablasts and memory B cells on maintaining the teleost humoral immune response. Upon resolving the mechanisms of affinityinduced teleost IgM isomerism and its humoral memory response, more cogent vaccine designs could be effectively developed and more precise system to evaluate the protective efficiency of vaccines will be established.