Centre for Inflammation Biology and Cancer Immunology, School of Immunology and Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, SE1 1UL, United Kingdom.
Published: August 2018
AI Article Synopsis
Article Abstract
A C1858T single nucleotide polymorphism within PTPN22 (which encodes PTPN22) is associated with an enhanced susceptibility to multiple autoimmune diseases including type 1 diabetes and rheumatoid arthritis. Many of the associated autoimmune diseases have an autoantibody component to their pathology. Fc receptors (FcRs) recognise autoantibodies when they bind to autoantigens and form immune complexes. After immune complex binding and receptor crosslinking, FcRs signal via Src and Syk family kinases, leading to antigen uptake, presentation and cytokine secretion. Ptpn22 encodes a protein tyrosine phosphatase that negatively regulates Src and Syk family kinases proximal to immunoreceptor signalling cascades. We therefore hypothesised that PTPN22 regulates immune complex stimulated FcR responses in dendritic cells (DCs). Bone marrow derived DCs (BMDCs) from wild type (WT) or Ptpn22 mice were pulsed with ovalbumin:anti-ovalbumin immune complexes (ova ICs). Co-culture with WT OT-II T cells revealed that ova IC pulsed Ptpn22 BMDCs have an enhanced capability to induce T cell proliferation. This was associated with an increased capability of Ptpn22 BMDCs to present immune complex derived antigens and to form ova IC dependent DC-T cell conjugates. These findings highlight PTPN22 as a regulator of FcR mediated responses and provide a link between the association of PTPN22 with autoantibody associated autoimmune diseases.
Background: Gastric cancer (GC) shows limited response to immune checkpoint inhibitors due to its complex tumor immune microenvironment (TIME). This study explores the functions of various immune cells in the complex TIME in GC.
Methods: We assessed CD8 + T-cell infiltration of GC tissues by immunohistochemistry, and performed single-cell RNA sequencing (scRNA-seq) of tumor and normal tissues from 34 patients with GC.
Division of Arthritis and Rheumatic Diseases, Oregon Health & Science University, Portland, OR, 97239, USA; Rheumatology Section, VA Portland Health Care System, Portland, OR, 97239, USA. Electronic address:
Rheumatoid arthritis (RA) is a chronic autoimmune disorder with a complex pathogenesis that evolves through various stages before clinical symptoms emerge. This review outlines the natural history of RA, starting from genetic predisposition and environmental triggers to preclinical autoimmunity and subsequent joint inflammation. Key genetic factors interact with environmental elements like smoking and infections, producing autoantibodies such as anti-citrullinated protein antibodies (ACPA) and rheumatoid factor, which precede clinical manifestations by several years.
A woman in her late 70s presented with a fever, rashes, and marked proximal muscle weakness. Noninfectious conditions, including myositis and vasculitis, were initially considered. Treatment with cephalosporins was ineffective, but the symptoms improved with minocycline, indicating possible Japanese spotted fever (JSF) despite no apparent history of tick exposure.
In this review, we aim to explore the multifaceted roles of galectins in host defense from a broader perspective, particularly regarding their functions when host integrity is compromised. Numerous comprehensive reviews on galectin functions in immunity have already been published. For researchers new to the field, this wealth of information may create an impression of galectins as proteins involved in a wide array of biological processes.
Department of Hematology, Taixing People's Hospital Affiliated to Yangzhou University, Taixing, China; Institute of Hematology, affiliated hospital of Yangzhou University, Taixing, China. Electronic address:
Acute myeloid leukemia (AML) is a complex hematological malignancy predominantly affecting the elderly, with a median diagnosis age of 68 years. Despite advances in treatment, elderly AML patients face suboptimal survival outcomes, with an estimated 5-year survival rate below 20 %. Epigenetic dysregulation, notably DNA methylation, is a key factor in the progression of myelodysplastic syndromes (MDS) to AML.
