Genes & Immunity

Journal Information
ISSN / EISSN : 1466-4879 / 1476-5470
Published by: Springer Nature (10.1038)
Total articles ≅ 1,680
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, Nina Janze, Ralph Goethe
Published: 25 October 2021
Interleukin-36α is a novel member of the IL-1 cytokine family that is highly expressed in epithelial tissues and several myeloid-derived cell types after induction. The transcription factor (TF) C/EBPβ binds specifically to an essential half-CRE•C/EBP motif in the Il36a promoter to induce Il36a expression upon LPS stimulation. C/EBPs regulate gene expression by binding to recognition sequences that can contain 5′-cytosine-phosphate-guanine-3′ dinucleotides (CpG), whose methylation can influence TF binding and gene expression. Herein we show that the half-CRE•C/EBP element in the Il36a promoter is differentially methylated in the murine RAW264.7 macrophage cell line and in primary murine macrophages. We demonstrate that C/EBPβ binding to the half-CRE•C/EBP element in the Il36a promoter following LPS stimulation is insensitive to CpG methylation and that methylation of the CpG in the half-CRE•C/EBP element does not alter LPS-induced Il36a promoter activity which correlated with similar Il36a mRNA copy numbers and pro-IL-36α protein amount in both cell types. Taken together, our data indicate that C/EBPβ binding to the half-CRE•C/EBP element and subsequent gene activation occurs independently of the CpG methylation status of the half-CRE•C/EBP motif and underlines the potential of C/EBPs to recognize methylated as well as unmethylated motifs.
, , Anna Dębińska, Grzegorz Myszczyszyn, Tomasz Szmatoła, Anna Myszkal, Igor Jasielczuk, Anna Drabik-Chamerska, Lidia Hirnle, Andrzej Boznański
Published: 12 October 2021
The publisher has not yet granted permission to display this abstract.
, , Chandana Basu Mallick, Rakesh Tamang, , Pratheusa Machha, Royana Singh, Abhishek Pathak, Vijay Nath Mishra, Pankaj Shrivastava, et al.
Published: 11 October 2021
The rapid expansion of coronavirus SARS-CoV-2 has impacted various ethnic groups all over the world. The burden of infectious diseases including COVID-19 are generally reported to be higher for the Indigenous people. The historical knowledge have also suggested that the indigenous populations suffer more than the general populations in the pandemic. Recently, it has been reported that the indigenous groups of Brazil have been massively affected by COVID-19. Series of studies have shown that many of the indigenous communities reached at the verge of extinction due to this pandemic. Importantly, South Asia also has several indigenous and smaller communities, that are living in isolation. Till date, despite the two consecutive waves in India, there is no report on the impact of COVID-19 for indigenous tribes. Since smaller populations experiencing drift may have greater risk of such pandemic, we have analysed Runs of Homozygosity (ROH) among South Asian populations and identified several populations with longer homozygous segments. The longer runs of homozygosity at certain genomic regions may increases the susceptibility for COVID-19. Thus, we suggest extreme careful management of this pandemic among isolated populations of South Asia.
Ann-Kathrin Mix, Griseldis Goob, Erik Sontowski,
Published: 29 September 2021
Genes & Immunity, Volume 22, pp 247-254;

Pathogenic bacteria have evolved a variety of highly selective adhesins allowing these microbes to engage specific surface determinants of their eukaryotic host cells. Receptor clustering induced by the multivalent microorganisms will not only anchor the bacteria to the tissue, but will inevitably trigger host cell signaling. It has become clear, that these bacteria-initiated signaling events can be seen as a form of localized communication with host epithelial cells. Such a microscale communication can have immediate consequences in the form of changes in host cell membrane morphology or cytoskeletal organization, but can also lead to transcriptional responses and medium- and long-term alterations in cellular physiology. In this review, we will discuss several examples of this form of microscale communication between bacterial pathogens and mammalian host cells and try to delineate their downstream ramifications in the infection process. Furthermore, we will highlight recent findings that specialized pathogenic bacteria utilize the adhesin-based interaction to diffuse the short-range messenger molecule nitric oxide into the host tissue. While anti-adhesive strategies to disrupt the initial bacterial attachment have not yet translated into medical applications, the ability to interfere with the microscale communication emanating on the host side provides an unconventional approach for preventing infectious diseases.
Samantha P. L. Law, Prudence N. Gatt, Stephen D. Schibeci, Fiona C. McKay, Steve Vucic, , Scott N. Byrne, David Brown, Graeme J. Stewart, Christopher Liddle, et al.
Published: 23 June 2021
Genes & Immunity, Volume 22, pp 227-233;

Although genetic and epidemiological evidence indicates vitamin D insufficiency contributes to multiple sclerosis (MS), and serum levels of vitamin D increase on treatment with cholecalciferol, recent metanalyses indicate that this vitamin D form does not ameliorate disease. Genetic variation in genes regulating vitamin D, and regulated by vitamin D, affect MS risk. We evaluated if the expression of vitamin D responsive MS risk genes could be used to assess vitamin D response in immune cells. Peripheral blood mononuclear cells (PBMCs) were isolated from healthy controls and people with MS treated with dimethyl fumarate. We assayed changes in expression of vitamin D responsive MS risk (VDRMS) genes in response to treatment with 25 hydroxy vitamin D in the presence or absence of inflammatory stimuli. Expression of CYP24A1 and other VDRMS genes was significantly altered in PBMCs treated with vitamin D in the homeostatic and inflammatory models. Gene expression in MS samples had similar responses to controls, but lower initial expression of the risk genes. Vitamin D treatment abrogated these differences. Expression of CYP24A1 and other MS risk genes in blood immune cells indicate vitamin D response and could enable assessment of immunological response to vitamin D in clinical trials and on therapy.
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