摘要
“Memories warm you up from the inside.But they also tear you apart.”―Haruki Murakami,Kafka on the Shore.One of the characteristics of the human immune system,in addition to the recognition of nonself pathogens and the tolerance of self-antigens,is its memory response to previously encountered pathogens and the mounting of a stronger,faster secondary response against these same antigens.A long-held paradigm in immunologic study in vertebrates is that immune memory is restricted to the adaptive immune response via memory T and B cells,which possess two distinct features:specificity(recognizing pathogen antigen fragments through surface receptors)and longevity(proliferation and long-term survival after the first encounter).1–3 Unlike adaptive immunity,the innate immune system exhibits a rapid response against pathogens and transforming cells without a previous encounter,and this response depends on a series of default genes and proteins expressed on cell surfaces and in the cytoplasm that recognize the pathogen-associated molecular patterns(PAMPs)of pathogens.Therefore,it was surprising to find several models of pathogen infections in invertebrates,including insects,worms,and jawless fish,that lack fully developed adaptive immunity but possess the features of antigen specificity and longevity likely involving phagocytic cells that can“recall”prior infection with limited specificity.In fact,immune memory has recently been described in vertebrate myeloid lineages,4 in which epigenetic changes are proposed to occur in macrophages previously stimulated through pattern recognition receptors.
