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The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Cutting Edge: Vitamin D-Mediated Human Antimicrobial Activity against Mycobacterium tuberculosis Is Dependent on the Induction of Cathelicidin

Liu, Philip T, Stenger, Steffen, Tang, Dominic H, Modlin, Robert L·2007·The Journal of Immunology

Abstract

Host defense against intracellular pathogens depends upon innate and adaptive antimicrobial effector pathways. TLR2/1-activation of monocytes leads to the vitamin D-dependent production of cathelicidin and, at the same time, an antimicrobial activity against intracellular Mycobacterium tuberculosis. To determine whether induction of cathelicidin was required for the vitamin D-triggered antimicrobial activity, the human monocytic cell line THP-1 was infected with M. tuberculosis H37Ra and then activated with the active vitamin D hormone 1,25-dihydroxyvitamin D3 (1,25D3). 1,25D3 stimulation resulted in antimicrobial activity against intracellular M. tuberculosis and expression of cathelicidin mRNA and protein. Using small interfering RNA (siRNA) specific for cathelicidin, 1,25D3-induced cathelicidin mRNA and protein expressions were efficiently knocked down, whereas a nonspecific siRNA control had little effect. Finally, 1,25D3-induced antimicrobial activity was completely inhibited in the presence of siRNA against cathelicidin, instead leading to enhanced intracellular growth of mycobacteria. These data demonstrate that cathelicidin is required for the 1,25D3-triggered antimicrobial activity against intracellular M. tuberculosis.

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Crossref · 10.4049/jimmunol.179.4.2060

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Metadata

Authors
Liu, P. T., Stenger, S., Tang, D. H., & Modlin, R. L.
Venue
The Journal of Immunology
Published
2007-08
Volume
179
Issue
4
Pages
2060-2063
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
OpenAlex
W1927671826
Cited by
773
References
2
FWCI
39.75
Type
journal article
Language
en
Open access
closed

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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