The etiological agent responsible for leprosy is Mycobacterium leprae, which survives and replicates within the vesicular system of macrophages

Explain the difference between tuberculoid leprosy and lepromatous leprosy in the context of T-cell differentiation and effector function.

What will be an ideal response?


Effective immune responses against intravesicular pathogens living in macrophages are mediated by TH1 cells rather than TH2 cells. In tuberculoid leprosy, the predominant effector T cells produced after infection are TH1 cells. These are effective in containing the infection, although they do not clear it completely. The disease is chronic and progresses slowly, and the damage to skin and peripheral nerves is caused mainly by the inflammatory responses initiated by activated macrophages. In lepromatous leprosy, in contrast, the predominant T cells produced are TH2 cells. Humoral immunity is induced, which results in the production of antibodies that are ineffective against intracellular bacteria. As a result, M. leprae replicates unchecked, causing severe tissue destruction and eventually the death of the patient.
Many factors influence the differentiation of CD4 T cells into TH1 or TH2 cells, including the cytokines produced by the antigen-presenting cells and leukocytes involved in the innate immune responses, the antigen concentration and peptide:MHC density, T-cell receptor affinity for peptide:MHC, and the cytokines produced by TH1 and TH2 cells themselves. If TH1 cells dominate an immune response, a cell-mediated immune response is favored. If TH2 cells dominate, a humoral immune response is favored.

Health & Biomechanics

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