1,721,097 research outputs found
Effect of induced pluripotent stem cell technology in blood banking
Population aging has imposed cost-effective alternatives to blooddonations. Artificial blood is still at the preliminary stages of development, and the need for viable cells seems unsurmountable. Because large numbers of viable cellsmust be promptly available for clinical use, stem cell technologies, expansion, and banking represent ideal tools to ensure a regular supply. Provided key donors can be identified, induced pluripotent stemcell (iPSC) technology could pave theway to a newera in transfusionmedicine, just as it is alreadydoing inmany other fields of medicine. The present review summarizes the current state of research on iPSC technology in the field of blood banking, highlighting hurdles, and promises
Comment on "Germinal center helper T cells are dual functional regulatory cells with suppressive activity to conventional CD4+ T cells"
http://www.jimmunol.org/content/179/2/731.1.ful
More on donor-derived T-cell leukemia after bone marrow transplantation
http://www.nejm.org/doi/full/10.1056/NEJMc06105
Gliptins
CORRISPONDENCE: As stated by Daniel Drucker and Michael Nauck,1 inhibitors of dipeptidyl peptidase 4 (DPP-4, “gliptins”) have been introduced into clinical practice for their ability to cleave and inactivate glucagon-like peptide 1 (GLP-1) and stimulate insulin secretion in type 2 diabetes mellitus.
Another interesting property of DPP-4 is potent inactivation of the chemokine CXCL12.2, 3 and 4 CXCL12 is thought to be central in the homing of haemopoietic stem cells (HSC) to bone marrow. By lowering CXCL12 catabolism, DPP-4 inhibition with gliptins is a promising strategy by which to improve HSC homing and increase engraftment efficiency after bone marrow transplantation. Preclinical models with other DPP-4 inhibitors5 support this notion.
Now, for the first time, haematologists have clinically approved DPP-4 inhibitors in their armamentarium. But clinical trials of gliptins have focused on diabetic patients and have not investigated their effect on HSC trafficking. Reduction in HSC counts in peripheral blood would be an expected consequence of diminished CXCL12 inactivation by DPP-4 after gliptin treatment. We do not know whether this effect occurs nor the concentrations of drug required to achieve it, so future clinical trials in recipients of HSC transplants should investigate this strategy. Conversely, it might be wise to avoid gliptins during treatment with granulocyte-colony stimulating factor for HSC mobilisation, in which the reverse of homing is desired.
We declare that we have no conflict of interest
Zika Virus: Implications for Public Health
The World Health Organization has declared the current Zika virus (ZIKV) epidemic a public health emergency of international concern. Lack of vaccines and reliable diagnostic tests, broad geographical distribution of mosquito species that can transmit the virus, and absence of population immunity in newly affected countries are causes for concern. Although most infected persons are asymptomatic, ZIKV has been associated with a rise in cases of neurological complications and fetal central nervous system malformations. This defines such an arbovirus as something whose transmission should be prevented. This review summarizes the current understanding of ZIKV biology and epidemiology, as well as possible interventions to prevent contagion and transmission
Checkpoint inhibitors and progressive multifocal leukoencephalopathy: friends of foes?
No abstract availabl
JC viremia and multiple sclerosis
Abstract
Following the development of progressive multifocal leukoencephalopathy (PML) in two multiple sclerosis (MS) patients treated with natalizumab and interferon-beta (IFNbeta), a possible correlation between JC virus (JCV), the etiological agent of PML, and MS has received heightened interest. In particular, attention has focused on assessing whether IFNbeta treatment could affect the replication of JCV and thus its frequency in the peripheral blood of MS patients and whether the presence of JCV DNA in peripheral blood could be a predictive marker of the risk of developing PML. In order to answer to these questions, peripheral blood samples were collected from 59 INFbeta-treated, 39 untreated relapsing-remitting MS patients, and 98 healthy controls (HCs) and JCV DNA levels were determined and quantified by means of a real-time polymerase chain reaction (Q-PCR) assay. Overall, no differences were found in the presence or viral load of JCV DNA of MS patients and the HCs, but JCV DNA was significantly less frequent in the peripheral blood of IFNbeta-treated patients (13.6%) compared to the untreated MS patients (46.1%) and the healthy controls (28.6%). These results suggest that the presence of JCV in the blood of MS patients cannot be considered as a marker or a risk factor for PML development. In addition, they indicate that treatment with INFbeta can lead to the reduction of presence of the JCV genome in the peripheral blood of MS patients and, thus, that this drug probably does not increase the risk of PML in MS patients treated with IFNbeta
Is SARS-CoV-2 Spike Evolution Being Retargeted at the N-Terminal Domain?
Since 2020, most of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) evolution has been focused on the receptor-binding domain (RBD) of the Spike protein. Nevertheless, the N-terminal domain (NTD) of Spike has been shown to represent the target for neutralizing antibodies, and accordingly, NTD mutations are relevant for immune escape. In 2024, after the introduction of the BA.2.86 saltation variant (heavily mutated at the NTD antigenic supersite), its descendant JN.1 has further explored NTD evolution in its progeny, largely focused on positions 22, 31, 59 and 60. In this review, we explore such convergent evolution in detail and hypothesize the underlying mechanisms
- …
