Aim: To clone human IL-1R II cDNA and construct its recombinant retrovirus vector so as to explore its role in IL-1R II related diseases.
Methods: Human IL-1R II cDNA was amplified by RT-PCR from peripheral blood mononuclear cells (PBMCs) and inserted into the vector PET22b to construct recombinant vector PET22b-IL-R II. The recombinant was transfected into E. coli BL21 and expressed under IPTG induction. Expressed products were detected by Western blot. In addition, human IL-1R-II cDNA was subcloned into retrovirus vector LZRSPBMN and transfected into 293 cells by calcium phosphate precipitation. IL-1R II expression was detected by immunohistochemical staining.
Results: IL-1R II cDNA with 1,203 bp was amplified by RT-PCR from human PBMCs. The recombinant of this cDNA could be expressed in E. coli,which was confirmed by Western blot results. Immunohistochemistry detection showed IL-1R II protein was expressed in 293 cells.
Conclusion: Human IL-1R II gene was cloned successfully. PET22b-IL-1R II and LZR-IL-1R II were constructed and the recombinant protein IL-1R II was expressed in E.coli BL21. The results reported herein lay the foundation for further research on the role of IL-1R II in certain diseases.
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Biomed Pharmacother
January 2025
Department of Molecular Science and Technology, Ajou University, Suwon 16499, Republic of Korea; S&K Therapeutics, Ajou University Campus Plaza 418, Worldcup-ro 199, Yeongton-gu, Suwon 16502, Republic of Korea. Electronic address:
Myeloid differentiation primary-response 88 (MyD88) is a crucial adaptor protein for initiating immune responses via Toll-like receptors (TLRs). This study employed a rational peptide design approach to develop MyD88 inhibitory peptides targeting the MyD88 interaction interface. The designed peptide, MyDIP2-4, was evaluated for its efficacy in inhibiting MyD88-dependent signaling in human and mouse cell lines.
View Article and Find Full Text PDFFront Immunol
December 2024
Duke Global Health Institute, Durham, NC, United States.
Introduction: Dysregulated host cytokine responses to SARS-CoV-2 infection are a primary cause of progression to severe disease, whereas early neutralizing antibody responses are considered protective. However, there are gaps in understanding the early temporal dynamics of these immune responses, and the profile of productive immune responses generated by non-hospitalized people with mild infections in the community.
Methods: Here we conducted a prospective cohort study of people with suspected infections/exposures in the US state of North Carolina, before vaccine availability.
J Dermatol Sci
December 2024
Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China. Electronic address:
Background: Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe adverse drug reactions with extensive keratinocyte death. Carbamazepine (CBZ), the most commonly implicated drug in SJS/TEN, is metabolized by the cytochrome P450 enzyme 3A4 (CYP3A4) into carbamazepine-10,11-epoxide (CBZE) in the liver. While CD8 cytotoxic T cells play an important role in SJS/TEN, the underlying mechanism of exuberant immune response by CD8 T cells in these conditions remains incompletely understood.
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October 2024
Vivian L. Smith Department of Neurosurgery, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Interleukin-1 Receptor Associated Kinase 1 (IRAK1) is a serine/threonine kinase that plays a critical role as a signaling transducer of the activated Toll-like receptor (TLR)/Interleukin-1 receptor (IL-1R) signaling pathway in both immune cells and cancer cells. Upon hyperphosphorylation by IRAK4, IRAK1 forms a complex with TRAF6, which results in the eventual activation of the NF-κB and MAPK pathways. IRAK1 can translocate to the nucleus where it phosphorylates STAT3 transcription factor, leading to enhanced IL-10 gene expression.
View Article and Find Full Text PDFCell Rep
November 2024
Laboratory of Molecular Genetics, Department of Immunology, Hellenic Pasteur Institute, 11521 Athens, Greece. Electronic address:
Microglia are strongly implicated in demyelinating neurodegenerative diseases with increasing evidence for roles in protection and healing, but the mechanisms that control CNS remyelination are poorly understood. Here, we show that microglia-specific deletion of tumor necrosis factor receptor 1 (TNFR1) and pharmacological inhibition of soluble TNF (solTNF) or downstream interleukin-1 receptor (IL-1R) allow maturation of highly activated disease-associated microglia with increased size and myelin phagocytosis capacity that accelerate cortical remyelination and motor recovery. Single-cell transcriptomic analysis of cortex at disease onset reveals that solTNF inhibition enhances reparative IL-10-responsive while preventing damaging IL-1-related signatures of disease-associated microglia.
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