| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3377880 | Journal of Microbiology, Immunology and Infection | 2015 | 6 Pages |
Abstract
The immunity of human immune cells and their ability to inhibit Mycobacterium tuberculosis (MTB) are key factors in the anti-MTB effect. However, MTB modulates the levels and activity of key intracellular second messengers, such as calcium, to evade protective immune responses. Recent studies suggest that inhibiting L-type calcium channel in immune cells using either antibodies or small interfering RNA increases calcium influx, upregulates the expression of proinflammation genes, and reduces MTB burden. First, we will review the key factors in calcium-signaling pathway that may affect the immunity of immune cells to MTB infection. Second, we will focus on the role of calcium channels in regulating cellular immunity to MTB. Finally, we will discuss the possibility of using calcium-channel blockers as anti-MTB chemotherapy drugs to enhance chemotherapy effects, shorten treatment period, and overcome drug resistance.
Related Topics
Life Sciences
Immunology and Microbiology
Immunology
Authors
Lele Song, Ruina Cui, Yourong Yang, Xueqiong Wu,