Biology subjects

Favier, B.

Publications and source records attributed to Favier, B..

3 recordsLinked to original sources

bioRxiv2021

LILRB1 and LILRB2 expression in peripheral blood immune cells at 18 and 24 months of age in infants born from mothers with placental malaria

BackgroundPlacental malaria (PM) is associated with a higher susceptibility of infants to Plasmodium falciparum (Pf) malaria. A hypothesis of immune tolerance has been suggested but no clear explanation has been provided so far. Our goal was to investigate the involvement of inhibitory receptors LILRB1 and LILRB2, known to drive immune evasion upon ligation with pathogen and/or host ligands, in PM-induced immune tolerance. MethodsInfants of mothers with or without PM were enrolled in Allada, southern Benin, and followed-up for 24 months. Antibodies with specificity for five blood stage parasite antigens were quantified by ELISA, and the frequency of immune cell subsets was quantified by flow cytometry. LILRB1 or LILRB2 expression was assessed on cells collected at 18 and 24 months of age. ResultsInfants born to PM-mothers had a higher risk of developing clinical malaria than those born to mothers without PM (IRR=1.53, p=0.040), and such infants displayed a lower frequency of non-classical monocytes (OR=0.74, p=0.01) that overexpressed LILRB2 (OR=1.36, p=0.002). Moreover, infants born to PM-mothers had lower levels of cytophilic IgG and higher levels of IL-10 during active infection. ConclusionModulation of IgG and IL-10 levels could impair monocyte functions (opsonisation/phagocytosis) in infants born to PM-mothers, possibly contributing to their higher susceptibility to malaria. The long-lasting effect of PM on infants monocytes was notable, raising questions about the capacity of ligands such as Rifins or HLA-I molecules to bind to LILRB1 and LILRB2 and to modulate immune responses, and about the reprogramming of neonatal monocytes/macrophages. KEY POINTSInfants of mothers with placental malaria were more susceptible to clinical malaria than those born to mothers without placental malaria and they displayed a lower frequency of non-classical monocytes that overexpressed LILRB2.

immunology↗

bioRxiv2021

Human gene function publications that describe wrongly identified nucleotide sequence reagents are unacceptably frequent within the genetics literature

Nucleotide sequence reagents underpin a range of molecular genetics techniques that have been applied across hundreds of thousands of research publications. We have previously reported wrongly identified nucleotide sequence reagents in human gene function publications and described a semi-automated screening tool Seek & Blastn to fact-check the targeting or non-targeting status of nucleotide sequence reagents. We applied Seek & Blastn to screen 11,799 publications across 5 literature corpora, which included all original publications in Gene from 2007-2018 and all original open-access publications in Oncology Reports from 2014-2018. After manually checking the Seek & Blastn screening outputs for over 3,400 human research papers, we identified 712 papers across 78 journals that described at least one wrongly identified nucleotide sequence. Verifying the claimed identities of over 13,700 nucleotide sequences highlighted 1,535 wrongly identified sequences, most of which were claimed targeting reagents for the analysis of 365 human protein-coding genes and 120 non-coding RNAs, respectively. The 712 problematic papers have received over 17,000 citations, which include citations by human clinical trials. Given our estimate that approximately one quarter of problematic papers are likely to misinform or distract the future development of therapies against human disease, urgent measures are required to address the problem of unreliable gene function papers within the literature. Author summaryThis is the first study to have screened the gene function literature for nucleotide sequence errors at the scale that we describe. The unacceptably high rates of human gene function papers with incorrect nucleotide sequences that we have discovered represent a major challenge to the research fields that aim to translate genomics investments to patients, and that commonly rely upon reliable descriptions of gene function. Indeed, wrongly identified nucleotide sequence reagents represent a double concern, as both the incorrect reagents themselves and their associated results can mislead future research, both in terms of the research directions that are chosen and the experiments that are undertaken. We hope that our research will inspire researchers and journals to seek out other problematic human gene function papers, as we are unfortunately concerned that our results represent the tip of a much larger problem within the literature. We hope that our research will encourage more rigorous reporting and peer review of gene function results, and we propose a series of responses for the research and publishing communities.

genetics↗

bioRxiv2017

Stage-specific ISG expression reveals functional convergence of type I and II IFNs in SIV infection

AbstractInterferons play a major role in controlling viral infections including HIV/SIV infections. Persistent up-regulation of interferon-stimulated-genes (ISGs) is associated with chronic immune activation and progression in SIV/HIV infections, but the respective contribution of different IFNs is unclear. We analyzed the expression of annotated IFN-induced genes in SIV-infected macaques to decrypt the respective roles of type-I (,{beta}) and type-II ({gamma}) IFNs. Both IFN types were induced in lymph nodes during early stage of primary infection. Induction of type-II IFN persisted during the chronic phase, in contrast to undetectable induction of type-I IFN. Interferome-based analysis of ISGs revealed that at both acute and chronic infection phases most differentially expressed ISGs were inducible by both type-I and type-II IFNs and displayed the highest increases, indicating strong convergence and synergy between type-I and type-II IFNs. The analysis of functional signatures of ISG expression revealed temporal changes in IFN expression patterns identifying phase-specific ISGs. These results suggest that IFN-{gamma} strongly contribute to shape ISG upregulation in addition to type-I IFN and may contribute to progression.

immunology↗