Abstract

Immunity to haemoprotozoa is complex, involving several components that interact in ways that vary from one host-parasite combination to another. In recent years, most attention has been given to antibody formation, which is relatively easily measured. It has been suggested that antibodies interfere with the penetration of merozoites into erythrocytes, or opsonize parasites or parasitized erythrocytes for phagocytosis by macrophages. Our observations on human and rodent malaria and Babesia infections show that other factors must also be borne in mind.Erythrocytes themselves differ in susceptibility to infection, and some of the factors underlying these differences are known, as will shortly be summarized. These differences are specific for each parasite, even though they do not depend upon acquired responses of immunocompetent cells.That both T- and B-lymphocytes respond to parasite antigens is, nevertheless, clear. Cells of the B-lymphocyte lineage produce antibodies to the parasites, and ways of detecting responses to T-lymphocytes are considered later.

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