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 ...
Mycobacterium tuberculosis (M. tb), is the known pathogen for causing tuberculosis. It infects appro...
Sustained calcium signaling in T cells is critical for development and activation. In this issue of ...
Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Author...
The immunity of human immune cells and their ability to inhibit Mycobacterium tuberculosis (MTB) are...
Mycobacterium tuberculosis modulates levels and activity of key intracellular second messengers to e...
Mycobacterium tuberculosis modulates levels and activity of key intracellular second messengers to e...
We demonstrated earlier the inhibitory role played by Voltage Gated Calcium Channels (VGCCs) in regu...
<div><p>The prevalence of <i>Mycobacterium tuberculosis</i> (<i>M</i>. <i>tb</i>) strains eliciting ...
<div><p>We demonstrated earlier the inhibitory role played by Voltage Gated Calcium Channels (VGCCs)...
Our previous work has demonstrated the roles played by L-type Voltage Gated Calcium Channels (VGCC) ...
The prevalence of Mycobacterium tuberculosis (M. tb) strains eliciting drug resistance has necessita...
<div><p>Our previous work has demonstrated the roles played by L-type Voltage Gated Calcium Channels...
T lymphocytes are an important part of the immune system that identify and destroy foreign antigens ...
Calcium is the most abundant mineral in the human body and is central to many physiological processe...
Tuberculosis (TB) remains a challenging global health concern and claims more than a million lives e...
Mycobacterium tuberculosis (M. tb), is the known pathogen for causing tuberculosis. It infects appro...
Sustained calcium signaling in T cells is critical for development and activation. In this issue of ...
Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Author...
The immunity of human immune cells and their ability to inhibit Mycobacterium tuberculosis (MTB) are...
Mycobacterium tuberculosis modulates levels and activity of key intracellular second messengers to e...
Mycobacterium tuberculosis modulates levels and activity of key intracellular second messengers to e...
We demonstrated earlier the inhibitory role played by Voltage Gated Calcium Channels (VGCCs) in regu...
<div><p>The prevalence of <i>Mycobacterium tuberculosis</i> (<i>M</i>. <i>tb</i>) strains eliciting ...
<div><p>We demonstrated earlier the inhibitory role played by Voltage Gated Calcium Channels (VGCCs)...
Our previous work has demonstrated the roles played by L-type Voltage Gated Calcium Channels (VGCC) ...
The prevalence of Mycobacterium tuberculosis (M. tb) strains eliciting drug resistance has necessita...
<div><p>Our previous work has demonstrated the roles played by L-type Voltage Gated Calcium Channels...
T lymphocytes are an important part of the immune system that identify and destroy foreign antigens ...
Calcium is the most abundant mineral in the human body and is central to many physiological processe...
Tuberculosis (TB) remains a challenging global health concern and claims more than a million lives e...
Mycobacterium tuberculosis (M. tb), is the known pathogen for causing tuberculosis. It infects appro...
Sustained calcium signaling in T cells is critical for development and activation. In this issue of ...
Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Author...