Cytokine patterns in leprosy lesions TNF-˜IFN-°IL-2 IL-4 IL-5 IL-10 Lepromatous TH2 cytokinesTH1 cytokines Lepromatous Tuberculoid Tuberculoid Lepromatous leprosy Organisms show ˜orid growth in macrophages High infectivity Hypergammaglobulinemia Disseminated infection. Bone, cartilage, and diffuse nerve damage Low or absent T-cell responsiveness. No response to M. leprae antigens Infection with Mycobacterium leprae can result in different clinical forms of leprosy There are two polar forms, tuberculoid and lepromatous leprosy, but several intermediate forms also exist Normal T-cell responsiveness. Speciÿc response to M. leprae antigens Tuberculoid leprosy Organisms present at low to undetectable levels Low infectivity Normal serum immunoglobulin levels Granulomas and local in˜ammation. Peripheral nerve damage
Like M. tuberculosis, M. leprae is able to persist and grow in macrophage vesicles and is normally restrained, but not cleared, by a type 1 host response. In patients who mount normal type 1 immune responses, few live bacteria are found, little antibody is produced, and, although skin and peripheral nerves are damaged by the inflammatory responses associated with macrophage activation, the disease progresses slowly and the patients typically survive. Because of its similarities to tuberculosis, this variant is called tuberculoid leprosy. This is in contrast to lepromatous leprosy, in which type 1 responses to M. leprae are deficient and an ineffective type 2 response is mounted instead. This results in abundant growth of the bacterium in macrophages and gross tissue destruction that is eventually fatal, if untreated. Although high levels of antibacterial antibodies are produced in patients with lepromatous leprosy, probably due to the high bacterial load, the antibodies are ineffective at controlling infection because they do not reach the intracellular bacteria.
13-21 Immune evasion is also practiced by protozoan parasites.
Most common protozoan parasites, such as Plasmodium and Trypanosoma species, have complex life cycles, part of which occurs in humans and part of which occurs in an intermediate host, such as an arthropod vector (for example, mosquitoes, flies, or ticks). The route of transmission of these organisms by their intermediate host is unusual, in that the normal barriers to infection are bypassed when the infectious agent is directly delivered to blood by a bite or the taking of a blood meal. Thus, many of the normal innate immune defenses associated with barrier function are completely bypassed during infection. Further, the most successful of these organisms have developed complex and varied immune evasion strategies that often result in ‘hideandseek’ chronic infections characterized by episodic disease manifestations, despite their eliciting antibody and cellmediated adaptive immune responses.