New Insights on the Role of TRP Channels in Calcium Signalling and Immunomodulation, 2020, 2021, Froghi et al

[Andy]

A review article, so probably nothing new in the ME section.

Full title: New Insights on the Role of TRP Channels in Calcium Signalling and Immunomodulation: Review of Pathways and Implications for Clinical Practice

Calcium is the most abundant mineral in the human body and is central to many physiological processes, including immune system activation and maintenance. Studies continue to reveal the intricacies of calcium signalling within the immune system. Perhaps the most well-understood mechanism of calcium influx into cells is store-operated calcium entry (SOCE), which occurs via calcium release-activated channels (CRACs). SOCE is central to the activation of immune system cells; however, more recent studies have demonstrated the crucial role of other calcium channels, including transient receptor potential (TRP) channels.

In this review, we describe the expression and function of TRP channels within the immune system and outline associations with murine models of disease and human conditions. Therefore, highlighting the importance of TRP channels in disease and reviewing potential. The TRP channel family is significant, and its members have a continually growing number of cellular processes. Within the immune system, TRP channels are involved in a diverse range of functions including T and B cell receptor signalling and activation, antigen presentation by dendritic cells, neutrophil and macrophage bactericidal activity, and mast cell degranulation. Not surprisingly, these channels have been linked to many pathological conditions such as inflammatory bowel disease, chronic fatigue syndrome and myalgic encephalomyelitis, atherosclerosis, hypertension and atopy.

Open access, https://link.springer.com/article/10.1007/s12016-020-08824-3

 

[mat]

Calcium signaling is also the mediator for Tachycardia in ME patients, am I mistaken?

 

[Trish]

This is the section on CFS:

Chronic Fatigue Syndrome

Chronic fatigue syndrome, also referred to as myalgic encephalomyelitis (ME) is a disorder identified by unexplained, debilitating fatigue accompanied by other neurological, immunological, autonomic and ion transport impairments [105, 106]. It has an unknown aetiology, and there are no specific diagnostic tests [107].

The most common finding reported in ME has been reduced NK cell cytotoxic activity [106, 107]. Atypical single nucleotide polymorphisms of the TRPM3 gene, from peripheral blood mononuclear cells, NK and B cells have been recently reported in ME groups compared with healthy controls [105, 106]. In addition, studies have shown a significantly reduced expression of TRPM3 on NK and B lymphocytes in ME patients [105]. This results in changes in Ca2+ ion concentration in the cytosol and intracellular stores which may change the NK cells’ activation threshold [106].

It appears to be based solely on one reference:

105.

Marshall-Gradisnik S et al (2016) Natural killer cells and single nucleotide polymorphisms of specific ion channels and receptor genes in myalgic encephalomyelitis/chronic fatigue syndrome. Appl Clin Genet 9:39–47