PubMed · 5192889
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J C Potier. 1969. [Immune tolerance].. https://pubmed.ncbi.nlm.nih.gov/5192889/
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In patients with severe and relapsing infections with non-tuberculous mycobacteria and Salmonella autosomal recessive as well as dominant-negative mutations are shown in genes for receptors of type-1 cytokines: the IL-12 receptor and the IFN-gamma receptor. In case of an impaired capacity to produce these cytokines or--given an abnormal receptor--to react to them, the cellular immune reaction does not run a normal course and the susceptibility to infection by intracellular pathogens is enhanced.
Patients suffering from lepromatous leprosy fail to develop an efficient cell-mediated immunity towards Mycobacterium leprae, the causative agent. The mechanism of such a specific T-cell tolerance to the bacillus remains a key question in the pathophysiology of leprosy. Macrophages do not show any intrinsic defect in phagocytizing and killing M. leprae or in presenting antigen to helper T-cells. On the other hand, M. leprae-reactive helper T-cells do persist in lepromatous patients, but their activation appears to prevented by active suppressor mechanisms, involving both suppressor T-cells and macrophages. The target of this specific suppression could be the interleukin 2-producing T-cell subset. A better molecular definition of M. leprae antigens, both by monoclonal antibodies and T-cell clones, should open new perspectives for further analysis of the regulation of immune responses to M. leprae.
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