Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Dr Jekyll and Mr Hyde: From Two Branches of Immune Response to Three Types of Interferon Response

Version 1 : Received: 4 August 2023 / Approved: 8 August 2023 / Online: 9 August 2023 (08:42:43 CEST)
Version 2 : Received: 23 September 2023 / Approved: 26 September 2023 / Online: 26 September 2023 (11:35:53 CEST)

How to cite: Brown, B. Dr Jekyll and Mr Hyde: From Two Branches of Immune Response to Three Types of Interferon Response. Preprints 2023, 2023080706. https://doi.org/10.20944/preprints202308.0706.v1 Brown, B. Dr Jekyll and Mr Hyde: From Two Branches of Immune Response to Three Types of Interferon Response. Preprints 2023, 2023080706. https://doi.org/10.20944/preprints202308.0706.v1

Abstract

Interferons were the original prototype cytokine system discovered during research of the 20th century. As the name suggests these were originally considered to be synthesised and secreted between cells. However, technological advancements since dictate processes involved in secreting these proteins can be extensively explained through both genetic and biochemical pathways comparatively clearer. Interferon (IFN) discovery occurred when genetic research was in its infancy. Simultaneous discovery by Franklin and Wilkins of deoxyribonucleic acid (DNA) structure and function occurred with Crick and Watson concurrently; however, two scientists Isaac and Lindemann described the first IFN in 1957. Technological advancement allows comparison, since many pathogens and genetic mutations can be factors in IFN regulation. Cancer cell regulation in research has long been central to host IFN synthesis and/or affected with differential IFN protein subunits defined further acting through 6 protein domains. Type II IFN remains central to immune cell function as it is released by a myriad of immune cells, mainly Natural Killer and T cells and is commonly used as a quantitative measurement of adaptive cellular immunity. Single–stranded and/or double–stranded RNA and DNA viruses as well as bacterial infections (e.g., Escherichia) and fungal infections (e.g., Mycobacteria) can affect IFN systems. These utilise intra/extracellular proteins like Toll–like Receptors (TLRs) affected by mutations within the overall IFN transduction pathways. Questions remain over immunological mechanisms contributing to innate and adaptive host immune regulation since type III IFN discovery in 2003 with immune cell phenotypes characterised further. Changes to synthesis of host type I/II/III IFNs may alter homeostatic cellular pathways differentially and beneficially in pathological disorders. We therefore aim to present the rationale of this regulatory protein mechanism of action in context with research developments recently with the functional effects

Keywords

Interferon, Innate, Adaptive, Genetic, Molecular

Subject

Biology and Life Sciences, Immunology and Microbiology

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