scholarly journals The mutual cooperation of blood platelets and lymphocytes in the development of autoimmune thyroid diseases

2018 ◽  
Vol 65 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Małgorzata Tomczyńska ◽  
Joanna Saluk-Bijak

Autoimmune thyroid diseases include several distinct clinical entities and mainly concern Graves` disease and Hashimoto's thyroiditis. An incompetent immune response directed against the body’s own tissues and the production of antibodies against specific cell antigens, accompanied by chronic inflammation occur in autoimmune thyroid diseases. The autoimmune process is induced by difficult to identify genetic and environmental factors, and generates the development of concomitant diseases of other systems. The inflammatory mediators, high level of thyroid hormones, lymphocyte activation and other immune cells play an important role in the chronic course of these diseases.  Autoimmune thyroid diseases are caused by disruptions of T-cells and other cells functions. The autoantibodies react with target antigens in different kinds of cells, including blood platelets. The autoimmune processes can cause the increased activity different kinds of cells including blood platelets and lymphocytes. The activity of blood platelets and lymphocytes is reciprocally regulated. It is suggested that blood platelets can influence lymphocyte function by direct contact through the receptors and via soluble mediators. The platelet–immune cell interactions represent a hallmark of immunity, as they can potently enhance immune cell functions.

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 665 ◽  
Author(s):  
Tiphaine C. Martin ◽  
Kristina M. Ilieva ◽  
Alessia Visconti ◽  
Michelle Beaumont ◽  
Steven J. Kiddle ◽  
...  

The pathogenesis of autoimmune thyroid diseases (AITD) is poorly understood and the association between different immune features and the germline variants involved in AITD are yet unclear. We previously observed systemic depletion of IgG core fucosylation and antennary α1,2 fucosylation in peripheral blood mononuclear cells in AITD, correlated with anti-thyroid peroxidase antibody (TPOAb) levels. Fucose depletion is known to potentiate strong antibody-mediated NK cell activation and enhanced target antigen-expressing cell killing. In autoimmunity, this may translate to autoantibody-mediated immune cell recruitment and attack of self-antigen expressing normal tissues. Hence, we investigated the crosstalk between immune cell traits, secreted proteins, genetic variants and the glycosylation patterns of serum IgG, in a multi-omic and cross-sectional study of 622 individuals from the TwinsUK cohort, 172 of whom were diagnosed with AITD. We observed associations between two genetic variants (rs505922 and rs687621), AITD status, the secretion of Desmoglein-2 protein, and the profile of two IgG N-glycan traits in AITD, but further studies need to be performed to better understand their crosstalk in AITD. On the other side, enhanced afucosylated IgG was positively associated with activatory CD335- CD314+ CD158b+ NK cell subsets. Increased levels of the apoptosis and inflammation markers Caspase-2 and Interleukin-1α positively associated with AITD. Two genetic variants associated with AITD, rs1521 and rs3094228, were also associated with altered expression of the thyrocyte-expressed ligands known to recognize the NK cell immunoreceptors CD314 and CD158b. Our analyses reveal a combination of heightened Fc-active IgG antibodies, effector cells, cytokines and apoptotic signals in AITD, and AITD genetic variants associated with altered expression of thyrocyte-expressed ligands to NK cell immunoreceptors. Together, TPOAb responses, dysregulated immune features, germline variants associated with immunoactivity profiles, are consistent with a positive autoreactive antibody-dependent NK cell-mediated immune response likely drawn to the thyroid gland in AITD.


2018 ◽  
Vol 22 (12) ◽  
pp. 6386-6390
Author(s):  
Małgorzata Tomczyńska ◽  
Ireneusz Salata ◽  
Michał Bijak ◽  
Joanna Saluk-Bijak

2014 ◽  
Author(s):  
Artur Bossowski ◽  
Hanna Borysewicz-Sanczyk ◽  
Natalia Wawrusiewicz-Kurylonek ◽  
Mieczyslaw Szalecki ◽  
Beata Wikiera ◽  
...  

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 255
Author(s):  
Wilmer Cuervo ◽  
Lorraine M. Sordillo ◽  
Angel Abuelo

Dairy calves are unable to mount an effective immune response during their first weeks of life, which contributes to increased disease susceptibility during this period. Oxidative stress (OS) diminishes the immune cell capabilities of humans and adult cows, and dairy calves also experience OS during their first month of life. However, the impact that OS may have on neonatal calf immunity remains unexplored. Thus, we aimed to evaluate the impact of OS on newborn calf lymphocyte functions. For this, we conducted two experiments. First, we assessed the association of OS status throughout the first month of age and the circulating concentrations of the cytokines interferon-gamma (IFN-γ) and interleukin (IL) 4, as well as the expression of cytokine-encoding genes IFNG, IL2, IL4, and IL10 in peripheral mononuclear blood cells (PBMCs) of 12 calves. Subsequently, we isolated PBMCs from another 6 neonatal calves to investigate in vitro the effect of OS on immune responses in terms of activation of lymphocytes, cytokine expression, and antibody production following stimulation with phorbol 12-myristate 13-acetate or bovine herpesvirus-1. The results were compared statistically through mixed models. Calves exposed to high OS status in their first month of age showed higher concentrations of IL-4 and expression of IL4 and IL10 and lower concentrations of IFN-γ and expression of IFNG and IL2 than calves exposed to lower OS. In vitro, OS reduced lymphocyte activation, production of antibodies, and protein and gene expression of key cytokines. Collectively, our results demonstrate that OS can compromise some immune responses of newborn calves. Hence, further studies are needed to explore the mechanisms of how OS affects the different lymphocyte subsets and the potential of ameliorating OS in newborn calves as a strategy to augment the functional capacity of calf immune cells, as well as enhance calves’ resistance to infections.


Author(s):  
Hanaa T. El‐Zawawy ◽  
Shwikar M. Ahmed ◽  
Eman A. El‐Attar ◽  
Asmaa A. Ahmed ◽  
Yara S. Roshdy ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document