Role of antibody dependent cell mediated cytotoxicity in ABO hemolytic disease of the newborn

1995 ◽  
Vol 62 (5) ◽  
pp. 587-592 ◽  
Author(s):  
Jayashree S. Patil ◽  
Snehalata C. Gupte
Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 376
Author(s):  
Chantal B. Lucini ◽  
Ralf J. Braun

In the last decade, pieces of evidence for TDP-43-mediated mitochondrial dysfunction in neurodegenerative diseases have accumulated. In patient samples, in vitro and in vivo models have shown mitochondrial accumulation of TDP-43, concomitantly with hallmarks of mitochondrial destabilization, such as increased production of reactive oxygen species (ROS), reduced level of oxidative phosphorylation (OXPHOS), and mitochondrial membrane permeabilization. Incidences of TDP-43-dependent cell death, which depends on mitochondrial DNA (mtDNA) content, is increased upon ageing. However, the molecular pathways behind mitochondrion-dependent cell death in TDP-43 proteinopathies remained unclear. In this review, we discuss the role of TDP-43 in mitochondria, as well as in mitochondrion-dependent cell death. This review includes the recent discovery of the TDP-43-dependent activation of the innate immunity cyclic GMP-AMP synthase/stimulator of interferon genes (cGAS/STING) pathway. Unravelling cell death mechanisms upon TDP-43 accumulation in mitochondria may open up new opportunities in TDP-43 proteinopathy research.


1989 ◽  
Vol 44 (5) ◽  
pp. 375-376
Author(s):  
H. A. A. BROUWERS ◽  
I. VAN ERTBRUGGEN ◽  
G. P. J. ALSBACH ◽  
E. F. VAN LEEUWEN ◽  
M. A. M. OVERBEEKE ◽  
...  

Vaccine ◽  
2012 ◽  
Vol 30 (48) ◽  
pp. 6753-6758 ◽  
Author(s):  
Workineh Torben ◽  
Gul Ahmad ◽  
Weidong Zhang ◽  
Stewart Nash ◽  
Loc Le ◽  
...  

Vox Sanguinis ◽  
1990 ◽  
Vol 58 (3) ◽  
pp. 231-231 ◽  
Author(s):  
Luis A. Carreras Vescio ◽  
Roberto A. Castro

2021 ◽  
Vol 23 (1) ◽  
pp. 17-34
Author(s):  
P. S. Obukhova ◽  
A. V. Kachanov ◽  
N. A. Pozdnyakova ◽  
M. M. Ziganshina

The mother and fetus incompatibility due to Rh-factor, blood group or other blood factors can lead to hemolytic disease of the fetus and newborn (HDN). HDN is a clinical disease condition of the fetus and newborn as a result of hemolysis, when maternal IgG alloantibodies cross the placenta and destroy the red blood cells of the fetus and newborn. The child disease begins in utero and can dramatically increase immediately after birth. As a result, hyperbilirubinemia and anemia develop, that can lead to abortions, serious complications, or death of the neonates in the absence of proper therapy. The range of HDN has changed significantly now compared to previous decades. Half a century ago, HDN was considered an almost complete synonym of RhD-alloimmunization, and this was a frequent problem for newborns. By now due to the high effective of Rh-conflict prevention, immunological AB0-conflicts have become the most common cause of HDN. The review aimes to one of the main causes of jaundice and anemia in neonates at present, i.e. HDN due to immunological AB0-conflict of mother and newborn (AB0-HDN). The main participants of the AВ0- incompatibility mother and child are considered, namely A- and B-glycans, as well as the corresponding anti-glycan alloantibodies. Close attention is paid to the structure features of glycan alloantigens on the red blood cells of the fetus and adult. The possible correlation of the frequency and severity of HDN with the blood group of mother and child, as well as with the titer of maternal alloantibodies, has been considered. The influence of immunoglobulin G subclasses on the AB0-HDN development has been evaluated. In most cases, AB0-HDN appear when the mother has the blood group 0, and the fetus has the group A (subgroup A1) or the group B. Other rare incidences of AB0-incompatibility with severe course are occurred. As a whole the etiology of AB0-HDN is complex and the HDN severity is influenced by many factors. The authors have analyzed statistical data, as well as the prevalence of AB0-incompatibility and AB0-HDN in various regions of the world. Current approaches to the diagnosis of AB0-HDN are discussed in addition. By now the problems of AB0- HDN occurrence and developing of ways to overcome this disease remain relevant.


2020 ◽  
Author(s):  
Wenyan Fu ◽  
Changhai Lei ◽  
Jian Zhao ◽  
Shi Hu

AbstractT cell immunoreceptor with Ig and ITIM domains (TIGIT) is a checkpoint receptor that mediates both T cell and natural killer (NK) cell exhaustion in tumours. An Fc-TIGIT fusion protein was shown to induce an immune-tolerance effect in a previous report, but the relevance of the TIGIT-Fc protein to tumour immunity is unknown. Here, we unexpectedly found that TIGIT-Fc promotes rather than suppresses tumour immunity. TIGIT-Fc treatment promoted the effector function of CD8+ T and NK cells in several tumour-bearing mouse models. Additionally, TIGIT-Fc treatment resulted in potent T cell and NK-cell-mediated tumour reactivity, sustained memory-induced immunity in tumour re-challenge models, enhanced therapeutic effects via an antibody against PD-L1, and induction of Th1 development in CD4+ T cells. TIGIT-Fc showed a potent antibody-dependent cell-mediated cytotoxicity (ADCC) effect but no intrinsic effect on tumour cell development. Our findings elucidate the unexpected role of TIGIT-Fc in tumour immune reprogramming, suggesting that TIGIT-Fc treatment alone or in combination with other checkpoint receptor blockers is a promising anticancer therapeutic strategy.


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