[Clinico-immunological study of the patients infected with Mycobacterium avium complex (MAC)]
Insights
Patients with Mycobacterium avium complex (MAC) infection show impaired lymphocyte proliferation. This decline is linked to reduced IL-2 production and monocyte suppression, affecting immune response.
Area of Science:
- Immunology
- Infectious Diseases
- Cell Biology
Context:
- Peripheral blood lymphocyte functions are crucial for immune response.
- Mycobacterium avium complex (MAC) infection affects various populations.
- Aging influences immune cell populations and function.
Purpose:
- To compare lymphocyte functions in MAC patients versus age-matched controls.
- To investigate the mechanisms underlying impaired lymphocyte proliferation in MAC patients.
Summary:
- Flow cytometry revealed lower total lymphocytes and T cell subsets, with higher natural killer cells in MAC patients compared to controls.
- Lymphocyte proliferation induced by PPD-S and PHA stimulation was significantly reduced in MAC patients.
- Recombinant IL-2 and monocyte depletion partially or fully restored PPD-S-induced proliferation, suggesting decreased IL-2 production and monocyte suppression.
Impact:
- Findings suggest a dual mechanism of impaired T cell immunity in MAC infection.
- Understanding these immune dysfunctions can inform therapeutic strategies for MAC patients.
- Highlights the impact of MAC infection on adaptive and innate immune cell balance.
Abstract:
Lymphocyte functions of the peripheral blood in the patients infected with MAC (MAC-pts) were evaluated comparatively with age-matched normal controls by using flow cytometry. The results obtained were as follows: 1) In normal controls, the number of total lymphocytes and the proportion and number of T lymphocyte subsets significantly decreased with age. The proportion of natural killer lymphocytes significantly increased in elder controls. 2) In MAC-pts, the number of total lymphocytes and T lymphocyte subsets were significantly lower and the proportion of natural killer lymphocytes were higher respectively than normal controls. 3) The lymphocyte proliferation induced by PPD-S stimulation in vitro in MAC-pts was significantly lower than the normal controls in both age groups of 50-69 and 70-89 years old. 4) The lymphocyte proliferation induced by PPD-S stimulation in MAC-pts was increased slightly by adding recombinant IL-2 and significantly higher by depletion of monocytes. By combination of both treatments, it recovered to the level of normal controls. From these results, we suggested that the decline of lymphocyte proliferation induced by PPD-S stimulation in MAC-pts was due to the decrease of IL-2 production by antigen committed lymphocytes and suppression by monocytes. 5) Lymphocyte proliferation induced by PHA stimulation in vitro was also significantly depressed in MAC-pts as compared with normal controls.
