scholarly journals Human Tissue-Resident Memory T Cells in the Maternal–Fetal Interface. Lost Soldiers or Special Forces?

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2699
Author(s):  
Caitlin S. DeJong ◽  
Nicholas J. Maurice ◽  
Stephen A. McCartney ◽  
Martin Prlic

The immune system plays a critical role during pregnancy, but the specific mechanisms and immune cell function needed to support pregnancy remain incompletely understood. Despite decades of research efforts, it is still unclear how the immune system maintains tolerance of fetal-derived tissues, which include most cells of the placenta and of course the fetus itself, without forfeiting the ability to protect against harmful infections. T cells recognize antigen in the context of major histocompatibility complex (MHC) encoded proteins, but classical MHC class I and II expression are diminished in fetal-derived cells. Can T cells present at the maternal–fetal interface (MFI) protect these cells from infection? Here we review what is known in regard to tissue-resident memory T (Trm) cells at the MFI. We mainly focus on how Trm cells can contribute to protection in the context of the unique features of the MFI, such as limited MHC expression as well as the temporary nature of the MFI, that are not found in other tissues.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Philip Newsholme

AbstractVarious nutrients can change cell structure, cellular metabolism, and cell function which is particularly important for cells of the immune system as nutrient availability is associated with the activation and function of diverse immune subsets. The most important nutrients for immune cell function and fate appear to be glucose, amino acids, fatty acids, and vitamin D. This perspective will describe recently published information describing the mechanism of action of prominent nutritional intervention agents where evidence exists as to their action and potency.


2009 ◽  
Vol 1209 ◽  
Author(s):  
Keyue Shen ◽  
Michael C Milone ◽  
Michael L. Dustin ◽  
Lance Cameron Kam

AbstractT lymphocytes are a key regulatory component of the adaptive immune system. Understanding how the micro- and nano-scale details of the extracellular environment influence T cell activation may have wide impact on the use of T cells for therapeutic purposes. In this article, we examine how the micro- and nano-scale presentation of ligands to cell surface receptors, including microscale organization and nanoscale mobility, influences the activation of T cells. We extend these studies to include the role of cell-generated forces, and the rigidity of the microenvironment, on T cell activation. These approaches enable delivery of defined signals to T cells, a step toward understanding the cell-cell communication in the immune system, and developing micro/nano- and material- engineered systems for tailoring immune responses for adoptive T cell therapies.


2016 ◽  
Author(s):  
Kyle Burrows ◽  
Frann Antignano ◽  
Michael Bramhall ◽  
Alistair Chenery ◽  
Sebastian Scheer ◽  
...  

ABSTRACTThe intestine is a unique immune environment that must respond to infectious organisms but remain tolerant to commensal microbes and food antigens. However, the molecular mechanisms that regulate immune cell function in the intestine remain unclear. Here we identify the POK/ZBTB family transcription factor Hypermethylated in cancer 1 (HIC1, ZBTB29) as a central component of immunity and inflammation in the intestine. HIC1 is specifically expressed in immune cells in the intestinal lamina propria (LP) in the steady state and mice with a T cell-specific deletion of HIC1 have reduced numbers of T cells in the LP. HIC1 expression is regulated by the Vitamin A metabolite retinoic acid, as mice raised on a Vitamin A-deficient diet lack HIC1-positive cells in the intestine. HIC1-deficient T cells overproduce IL-17A in vitro and in vivo, and fail to induce intestinal inflammation, identifying a critical role for HIC1 in the regulation of T cell function in the intestinal microenvironment under both homeostatic and inflammatory conditions.


2019 ◽  
Vol 216 (5) ◽  
pp. 1214-1229 ◽  
Author(s):  
Lalit K. Beura ◽  
Nancy J. Fares-Frederickson ◽  
Elizabeth M. Steinert ◽  
Milcah C. Scott ◽  
Emily A. Thompson ◽  
...  

This study examines the extent to which memory CD4+ T cells share immunosurveillance strategies with CD8+ resident memory T cells (TRM). After acute viral infection, memory CD4+ T cells predominantly used residence to survey nonlymphoid tissues, albeit not as stringently as observed for CD8+ T cells. In contrast, memory CD4+ T cells were more likely to be resident within lymphoid organs than CD8+ T cells. Migration properties of memory-phenotype CD4+ T cells in non-SPF parabionts were similar, generalizing these results to diverse infections and conditions. CD4+ and CD8+ TRM shared overlapping transcriptional signatures and location-specific features, such as granzyme B expression in the small intestine, revealing tissue-specific and migration property–specific, in addition to lineage-specific, differentiation programs. Functionally, mucosal CD4+ TRM reactivation locally triggered both chemokine expression and broad immune cell activation. Thus, residence provides a dominant mechanism for regionalizing CD4+ T cell immunity, and location enforces shared transcriptional, phenotypic, and functional properties with CD8+ T cells.


2020 ◽  
Vol 32 (9) ◽  
pp. 583-587 ◽  
Author(s):  
Changwei Peng ◽  
Stephen C Jameson

Abstract Independent studies over the last decade have characterized the properties of non-circulating CD8+ ‘resident’ memory T cells (TRM), which offer barrier protective immunity in non-lymphoid tissues and CD4+ follicular helper T cells (TFH), which mediate B-cell help in lymphoid sites. Despite their very different biological roles in the immune system, intriguing parallels have been noted between the trafficking properties and differentiation cues of these populations, parallels which have only sharpened with recent findings. In this review, we explore the features that underlie these similarities and discuss whether these indicate meaningful homologies in the development of CD8+ TRM and CD4+ TFH or reflect resemblances which are only ‘skin-deep’.


Hypertension ◽  
2020 ◽  
Vol 75 (2) ◽  
pp. 372-382 ◽  
Author(s):  
John Henry Dasinger ◽  
Ammar J. Alsheikh ◽  
Justine M. Abais-Battad ◽  
Xiaoqing Pan ◽  
Daniel J. Fehrenbach ◽  
...  

The SS (Dahl salt sensitive) rat is an established model of hypertension and renal damage that is accompanied with immune system activation in response to a high-salt diet. Investigations into the effects of sodium-independent and dependent components of the diet were shown to affect the disease phenotype with SS/MCW (JrHsdMcwi) rats maintained on a purified diet (AIN-76A) presenting with a more severe phenotype relative to grain-fed SS/CRL (JrHsdMcwiCrl) rats. Since contributions of the immune system, environment, and diet are documented to alter this phenotype, this present study examined the epigenetic profile of T cells isolated from the periphery and the kidney from these colonies. T cells isolated from kidneys of the 2 colonies revealed that transcriptomic and functional differences may contribute to the susceptibility of hypertension and renal damage. In response to high-salt challenge, the methylome of T cells isolated from the kidney of SS/MCW exhibit a significant increase in differentially methylated regions with a preference for hypermethylation compared with the SS/CRL kidney T cells. Circulating T cells exhibited similar methylation profiles between colonies. Utilizing transcriptomic data from T cells isolated from the same animals upon which the DNA methylation analysis was performed, a predominant negative correlation was observed between gene expression and DNA methylation in all groups. Lastly, inhibition of DNA methyltransferases blunted salt-induced hypertension and renal damage in the SS/MCW rats providing a functional role for methylation. This study demonstrated the influence of epigenetic modifications to immune cell function, highlighting the need for further investigations.


2021 ◽  
Vol 97 (3) ◽  
pp. 158-166
Author(s):  
Tünde Várvölgyi ◽  
◽  
Andrea Szegedi

The prevalence of vitiligo is between 0.5% and 1% in the population, the most common acquired depigmentation disorder. Hypopigmented macules are formed as a result of melanocyte death. Its etiology is still not fully elucidated, it is a multifactorial disease. Polygenic type genetic susceptibility is supported by familial accumulation (15- 30%). The complex interaction of non-immunological and immunological factors is key during the development of the disease. Due to intensive research in recent years, it has become clear that cells other than melanocytes, such as keratinocytes, fibroblasts, natural killer (NK) cells, and other cells of the innate immune system are involved in its pathogenesis. Furthermore, a special group of T lymphocytes, the tissue-resident memory T cells, play a key role also in the development and recurrence of the disease. The aim of the treatment is to stop progression, to achieve repigmentation, which is transient in 40% of cases.


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