Publication | Open Access
Pulmonary tuberculosis patients with a vitamin D deficiency demonstrate low local expression of the antimicrobial peptide LL-37 but enhanced FoxP3+ regulatory T cells and IgG-secreting cells
54
Citations
45
References
2014
Year
Pulmonary TuberculosisT-regulatory CellHumoral ResponseImmune RegulationImmunologyHuman TuberculosisPulmonary Tuberculosis PatientsTuberculosisAutoimmunityT Cell ImmunityCd4 T Cell ResponsesAntimicrobial Peptide Ll-37Vitamin D DeficiencyTb LesionsImmunopathologyImmune SystemMedicineIgg-secreting Cells
Control of human tuberculosis (TB) requires induction and maintenance of both macrophage and T cell effector functions. We demonstrate that pulmonary TB patients with a vitamin D deficiency had significantly reduced local levels of the vitamin D-inducible antimicrobial peptide LL-37 in granulomatous lesions compared to distal parenchyma from the infected lung. Instead, TB lesions were abundant in CD3(+) T cells and FoxP3(+) regulatory T cells as well as IgG-secreting CD20(+) B cells, particularly in sputum-smear positive patients with cavitary TB. Mycobacteria-specific serum IgG titers were also elevated in patients with active TB. An up-regulation of the B cell stimulatory cytokine IL-21 correlated with mRNA expression of CD20, total IgG and also IL-10 in the TB lesions. Altogether, vitamin D-deficient TB patients expressed a weak antimicrobial response but an IL-21 associated expansion of IgG-secreting B cells combined with a rise in FoxP3(+) regulatory T cells at the local site of infection.
| Year | Citations | |
|---|---|---|
Page 1
Page 1