In immunology, autoimmunity is the system of immune responses of an organism against its own healthy cells, tissues and other normal body constituents. Any disease resulting from this type of immune response is termed an "autoimmune disease". Prominent examples include celiac disease, diabetes mellitus type 1, Henoch–Schönlein purpura, systemic lupus erythematosus, Sjögren syndrome, eosinophilic granulomatosis with polyangiitis, Hashimoto's thyroiditis, Graves' disease, idiopathic thrombocytopenic purpura, Addison's disease, rheumatoid arthritis, ankylosing spondylitis, polymyositis, dermatomyositis, and multiple sclerosis. Autoimmune diseases are very often treated with steroids.
A dendritic cell (DC) is an antigen-presenting cell of the mammalian immune system. A DC's main function is to process antigen material and present it on the cell surface to the T cells of the immune system. They act as messengers between the innate and adaptive immune systems.
An immune complex, sometimes called an antigen-antibody complex or antigen-bound antibody, is a molecule formed from the binding of multiple antigens to antibodies. The bound antigen and antibody act as a unitary object, effectively an antigen of its own with a specific epitope. After an antigen-antibody reaction, the immune complexes can be subject to any of a number of responses, including complement deposition, opsonization, phagocytosis, or processing by proteases. Red blood cells carrying CR1-receptors on their surface may bind C3b-coated immune complexes and transport them to phagocytes, mostly in liver and spleen, and return to the general circulation.
Immune tolerance, also known as immunological tolerance or immunotolerance, refers to the immune system's state of unresponsiveness to substances or tissues that would otherwise trigger an immune response. It arises from prior exposure to a specific antigen and contrasts the immune system's conventional role in eliminating foreign antigens. Depending on the site of induction, tolerance is categorized as either central tolerance, occurring in the thymus and bone marrow, or peripheral tolerance, taking place in other tissues and lymph nodes. Although the mechanisms establishing central and peripheral tolerance differ, their outcomes are analogous, ensuring immune system modulation.
Plasmacytoid dendritic cells (pDCs) are a rare type of immune cell that are known to secrete large quantities of type 1 interferon (IFNs) in response to a viral infection. They circulate in the blood and are found in peripheral lymphoid organs. They develop from bone marrow hematopoietic stem cells and constitute < 0.4% of peripheral blood mononuclear cells (PBMC). Other than conducting antiviral mechanisms, pDCs are considered to be key in linking the innate and adaptive immune systems. However, pDCs are also responsible for participating in and exacerbating certain autoimmune diseases like lupus. pDCs that undergo malignant transformation cause a rare hematologic disorder, blastic plasmacytoid dendritic cell neoplasm.
Cluster of Differentiation 86 is a protein constitutively expressed on dendritic cells, Langerhans cells, macrophages, B-cells, and on other antigen-presenting cells. Along with CD80, CD86 provides costimulatory signals necessary for T cell activation and survival. Depending on the ligand bound, CD86 can signal for self-regulation and cell-cell association, or for attenuation of regulation and cell-cell disassociation.
OX40L is the ligand for OX40 and is stably expressed on many antigen-presenting cells such as DC2s, macrophages, and activated B lymphocytes.
B-cell activating factor (BAFF) also known as tumor necrosis factor ligand superfamily member 13B and CD257 among other names, is a protein that in humans is encoded by the TNFSF13B gene. BAFF is also known as B Lymphocyte Stimulator (BLyS) and TNF- and APOL-related leukocyte expressed ligand (TALL-1) and the Dendritic cell-derived TNF-like molecule.
Fms-related tyrosine kinase 3 ligand (FLT3LG) is a protein which in humans is encoded by the FLT3LG gene.
Interferon alpha-1 is a protein that in humans is encoded by the IFNA1 gene.
Dedicator of cytokinesis protein 2 (Dock2) is a protein encoded in the human by the DOCK2 gene. Dock2 is a large protein involved in intracellular signalling networks. It is a member of the DOCK-A subfamily of the DOCK family of guanine nucleotide exchange factors (GEFs) which function as activators of small G-proteins. Dock2 specifically activates isoforms of the small G protein Rac.
Lymphocyte-activation gene 3, also known as LAG-3, is a protein which in humans is encoded by the LAG3 gene. LAG3, which was discovered in 1990 and was designated CD223 after the Seventh Human Leucocyte Differentiation Antigen Workshop in 2000, is a cell surface molecule with diverse biological effects on T cell function but overall has an immune inhibitory effect. It is an immune checkpoint receptor and as such is the target of various drug development programs by pharmaceutical companies seeking to develop new treatments for cancer and autoimmune disorders. In soluble form it is also being developed as a cancer drug in its own right.
Fc fragment of IgG receptor IIb is a low affinity inhibitory receptor for the Fc region of immunoglobulin gamma (IgG). FCGR2B participates in the phagocytosis of immune complexes and in the regulation of antibody production by B lymphocytes.
Lupus, formally called systemic lupus erythematosus (SLE), is an autoimmune disease in which the body's immune system mistakenly attacks healthy tissue in many parts of the body. Symptoms vary among people and may be mild to severe. Common symptoms include painful and swollen joints, fever, chest pain, hair loss, mouth ulcers, swollen lymph nodes, feeling tired, and a red rash which is most commonly on the face. Often there are periods of illness, called flares, and periods of remission during which there are few symptoms. Children up to 18 years old develop a more severe form of SLE termed childhood-onset systemic lupus erythematosus.
Piezo-type mechanosensitive ion channel component 1 is a protein that in humans is encoded by the PIEZO1 gene. PIEZO1 is a large mechanosensitive ion channel protein that forms a homotrimeric complex with a distinctive three-bladed, propeller-shaped architecture. Each subunit of PIEZO1 contains between 30 and 40 transmembrane domains. The protein consists of a central pore module and peripheral mechanotransduction modules. The pore module is composed of the last two transmembrane helices, an extracellular cap domain, and an intracellular C-terminal domain.
Gunther Hartmann is a German immunologist and clinical pharmacologist. Since 2007 he has been the Director of the Institute of Clinical Chemistry and Clinical Pharmacology at the University Hospital of the University of Bonn.
Jacques Banchereau is an internationally prominent French American immunologist and molecular biologist. As of 2024, he is Chief Scientific Officer at Javelin Biotech. He was formerly professor and director of immunological sciences at the Jackson Laboratory for Genomic Medicine and also the former chief science officer, senior vice president, and DTA head of inflammation & virology at Hoffman-La Roche. He is best known for his extensive research on dendritic cells with Nobel Laureate Ralph M. Steinman. He is the fifth most cited immunologist ranked by Times Higher Education's report.
Miram Merad is a French-Algerian professor in Cancer immunology and the Director of the Marc and Jennifer Lipschultz Precision Immunology Institute (PrIISM) at the Icahn School of Medicine at Mount Sinai (ISMMS) in New York, NY. She is the corecipient of the 2018 William B. Coley Award for Distinguished Research in Basic Immunology and a member of the United States National Academy of Sciences and the National Academy of Medicine.
Carla V. Rothlin is an Argentinian immunologist. She is a professor of immunobiology at Yale University, where she holds the Dorys McConnell Duberg Professorship, and also serves as a professor of pharmacology. Rothlin is the co-leader of the Cancer Immunology Program at Yale Cancer Center and a Howard Hughes Medical Investigator Faculty Scholar.
Elina Zúñiga is an Argentinian Immunologist and Professor of Molecular Biology in the Division of Biological Sciences at the University of California, San Diego. Zúñiga has made critical discoveries regarding host-virus interactions in both acute and chronic infections. Using lymphocytic choriomeningitis models (LCMV) and murine cytomegalovirus models, her laboratory at UCSD studies host immune adaptations in chronic viral disease and methods of viral suppression of the immune system in order to develop novel methods and identify novel targets of anti-viral defence. In 2018, Zúñiga was chosen by the American Association of Immunologists to give the international Vanguard Lecture. Zúñiga is also co-founder of the Global Immunotalks series which she and Carla Rothlin started in 2020 as a means to make cutting-edge immunology research freely available and easily accessible to a global audience.
