Teilah Huth

Source:Griffith Health Institute

Teilah Kathryn Huth, PhD, is a researcher at the National Centre for Neuroimmunology and Emerging Diseases (NCNED) at Griffith University, Australia. Her primary interest is in investigating the role of Natural Killer (NK) cells in ME/CFS and why the function of NK cells has been found to be reduced in patients with ME/CFS.

Doctorate thesis

• 2016, Investigation of Cellular and Genetic Mechanisms Required for Natural Killer Cell Cytotoxic Activity in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis - (Thesis Full Text)

Notable studies

• 2013, Measurement of natural killer cell apoptotic inducing lytic proteins in peripheral blood mononuclear cells and isolated natural killer cells - (Abstract)
• 2013, The role of Dendritic Cells and Monocytes in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis - (Abstract)
• 2014, The Role of Adaptive and Innate Immune Cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis - (Full Text)
• 2014, Analysis of the Relationship between Immune Dysfunction and Symptom Severity in Patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) - (Full Text)
• 2014, Characterization of Natural Killer Cell Phenotypes in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis - (Full Text)
• 2015, Characterisation of cell functions and receptors in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) - (Full Text)
• 2015, Longitudinal analysis of immune abnormalities in varying severities of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients - (Full Text)
• 2015, Serum Immune Proteins in Moderate and Severe Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients - (Full Text)
• 2016, ERK1/2, MEK1/2 and p38 downstream signalling molecules impaired in CD56dimCD16+ and CD56brightCD16dim/− natural killer cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients - (Full Text)
• 2016, Killer Cell Immunoglobulin-like Receptor Genotype and Haplotype Investigation of Natural Killer Cells from an Australian Population of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients -(Full Text)
• 2016, Natural killer cells and single nucleotide polymorphisms of specific ion channels and receptor genes in myalgic encephalomyelitis/chronic fatigue syndrome - (Full Text)
• 2016, Pilot Study of Natural Killer Cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and Multiple Sclerosis - (Abstract)

See also

• National Centre for Neuroimmunology and Emerging Diseases

myalgic encephalomyelitis (M.E.) - A disease often marked by neurological symptoms, but fatigue is sometimes a symptom as well. Some diagnostic criteria distinguish it from chronic fatigue syndrome, while other diagnostic criteria consider it to be a synonym for chronic fatigue syndrome. A defining characteristic of ME is post-exertional malaise (PEM), or post-exertional neuroimmune exhaustion (PENE), which is a notable exacerbation of symptoms brought on by small exertions. PEM can last for days or weeks. Symptoms can include cognitive impairments, muscle pain (myalgia), trouble remaining upright (orthostatic intolerance), sleep abnormalities, and gastro-intestinal impairments, among others. An estimated 25% of those suffering from ME are housebound or bedbound. The World Health Organization (WHO) classifies ME as a neurological disease.

apoptosis a type of cell death in which a cell, in response to a threat, initiates a series of molecular steps that lead to its orderly death. This is one method the body uses to get rid of unneeded or abnormal cells. This form of cell suicide is also called programmed cell death.

serum The clear yellowish fluid that remains from blood plasma after clotting factors have been removed by clot formation. (Blood plasma is simply blood that has had its blood cells removed.)

antibodies Antibody/immunoglobulin refers to any of a large number of specific proteins produced by B cells that act against an antigen in an immune response.

single nucleotide polymorphism (SNP) - A single nucleotide polymorphism (SNP, pronounced "snip") is a potential genetic mutation that occurs in a single spot in the human genome; a difference in a single DNA building block. SNPs are often represented by an "rs" number, such as "rs53576".