Abstract
Type 1 CD4+ T helper (Th1) cells mediate resistance to Mycobacterium tuberculosis (Mtb), and Th2 immunity generates specific immunoglobulin E upon allergen exposure. We investigated the impact of active tuberculosis (TB), atopic status, and anti-TB treatment on the balance between Th1 and Th2 (type 2 CD4+ T helper) immunity. CD4+/interferon (IFN)-γ+ Th1 cells (%Th1) and CD4+/interleukin-4+ Th2 cells (%Th2) in bronchoalveolar lavage (BAL) fluid and peripheral blood mononuclear cells (PBMCs) were measured by flow cytometry. The BAL %Th1 was higher in TB patients at baseline, compared to that in non-TB subjects, and was further increased in TB patients after stimulation with phorbol myristate acetate and ionomycin. The stimulated BAL %Th1 was inversely correlated with the severity score of chest radiography in TB patients. Heat-killed Mtb triggered more IFN-γ and nitrite production, as determined by enzyme-linked immunosorbent assay and the Griess reaction, respectively, from the alveolar macrophages of TB patients than that of non-TB subjects. Non-atopic TB participants had a higher %Th1 in PBMCs, compared to atopic individuals, and their %Th1 decreased after 3-month anti-TB treatment. Th1 response is provoked by active TB infection, is associated with less severe radiographic changes, is reduced in atopic patients with active TB infection, and is attenuated after anti-TB treatment.
Highlights
Among the TB patients, the cellularity of the bronchoalveolar lavage (BAL) fluid was significantly higher in the non-atopic TB patients, compared to that of the atopic TB patients
There was no difference in the proportion of eosinophils in the BAL fluid between
Host immunity against Mycobacterium tuberculosis (Mtb) infection has often been described as being orchestrated by Th1 cells [4]
Summary
CD4+ T-helper (Th) cells orchestrate the immune system through the production of cytokines [1]. Upon exposure to intracellular microorganisms and allergens, macrophages and dendritic cells process these antigens and present them to naïve T cells, directing the differentiation of interferon (IFN)-γ+ type 1 CD4+ T helper (Th1) cells and interleukin (IL)-4+ type 2 CD4+ T helper (Th2) cells, respectively. These Th cells antagonize each other and are modulated by regulatory T cells. The imbalance of Th cell cytokines is likely to determine clinical outcomes
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