Immunology of Beta Cells and Inflammation

Immune cells that release substances called chemokines which attract other immune cells to the site of inflammation.

Beta cells start releasing CCL2 and CXCL10, attracting neutrophils and monocytes (which mature into macrophages) and specific types of T cells called TH1 and CD8 T cells.

Stress ligands expressed on beta cells that activate NK cells, leading to their destruction.

A process where the immune response to an initial antigen spreads to other related antigens, leading to a broader attack.

Macrophages present processed antigens from destroyed beta cells to T cells, activating other T cell clones to attack beta cells.

Antigens that are normally hidden within cells and become exposed to the immune system when those cells are damaged or destroyed.

A type of autoimmune disease characterized by blistering on the skin and mucous membranes, specifically in the mouth.

A protein found in the buccal mucosa (mouth lining) that is targeted by antibodies in the initial stages of pemphigus.

A protein similar to alpha-desmoglein 3, but more abundant in the skin, targeted by antibodies in later stages of pemphigus.

The mechanism by which an autoimmune disease progresses and its cause is investigated.

An enzyme expressed by beta cells of the pancreas that is targeted by lymphocytes in type 1 diabetes.

A type of autoimmune disease characterized by the destruction of insulin-producing beta cells in the pancreas, leading to insulin deficiency.

The immune system's response to an infection can sometimes mistakenly target the body's own cells and tissues, leading to autoimmune disease.

Immune cells, like dendritic cells, play a crucial role in triggering the immune response by recognizing and presenting antigens to T cells and B cells.

The release of self-antigens, like proteins and nucleic acids, from damaged cells can activate the immune system against the body's own tissues.

The process in which an antigen from a pathogen closely resembles a self-antigen, tricking the immune system into attacking the body's own tissues.

Interferons, especially interferon type 1 and interferon gamma, are crucial cytokines involved in antiviral responses and autoimmune disease pathogenesis.

The activation of the immune system against self-antigens leads to the production of autoreactive T cells and B cells, which contribute to autoimmune disease.

Autoantibodies are antibodies produced by B cells that mistakenly target self-antigens, contributing to tissue damage and autoimmune disease.

MHC molecules, specifically MHC class 1 and 2, play a crucial role in presenting antigens to T cells, and their dysregulation can contribute to autoimmune disease.

PAMPs are molecules found on pathogens that trigger an immune response in the body. They are recognized by phagocytes, which are immune cells that engulf and destroy pathogens.

During an infection, phagocytes migrate to lymph nodes, where they can activate other immune cells, including T cells. However, this activation can sometimes be non-specific, leading to the activation of T cells that are not specific to the pathogen.

During an infection, the inflammatory environment can activate both specific T cells that recognize the pathogen and non-specific T cells, due to the release of cytokines. This non-specific activation is called the bystander effect.

Regulatory T cells (Tregs) are a type of immune cell that help to suppress the immune response and prevent autoimmune diseases. However, during infection, the inflammatory environment suppresses Treg function.

Pro-inflammatory cytokines released during infection suppress the function of regulatory T cells (Tregs). This means the Treg cells are unable to release their usual inhibitory cytokines, such as TGFβ, IL10, and IL35.

The inflammatory response during infection can create an environment that promotes the development of autoimmune diseases. This is because Tregs are suppressed, allowing autoreactive T cells to become activated.

Dendritic cells are immune cells that play a role in presenting antigens to other immune cells. In autoimmune diseases, dendritic cells accumulate in areas of inflammation, contributing to the disease process.

Targeting and eliminating dendritic cells in the joints can effectively reduce the symptoms of autoimmune diseases. This suggests that dendritic cells play a crucial role in the development and progression of these diseases.

Tumor-specific antigens are proteins uniquely present on tumor cells and absent in normal cells. These antigens are targeted by the immune system, leading to tumor rejection.

Tumor-associated antigens (TAAs) are proteins found in both normal cells and tumor cells, but their expression patterns differ. These antigens can be upregulated, expressed in the wrong cell type, or expressed at the wrong time in tumor cells.

The rejection of a tumor transplant in a normal mouse injected with lymphocytes from the original tumor-bearing mouse indicates that the immune system is recognizing tumor-specific antigens on the tumor cells.

The immune response to TAA involves T cells recognizing these altered proteins on the MHC complex of tumor cells.

TAAs can be identified by comparing the protein profiles of tumor cells and normal cells. Any aberrantly expressed proteins are potential TAAs.

Genetic approaches involve co-culturing tumor cells with lymphocytes, which allows for the expansion of specific T cells recognizing TAAs on the tumor cells.

By isolating T cells that are specific for tumor antigens, researchers can identify the corresponding TAAs that trigger this immune response.

The identification of TAAs is crucial for developing targeted therapies. These therapies aim to stimulate the patient's immune system to target and destroy tumor cells.

Antibody-dependent cellular cytotoxicity (ADCC) is a process where antibodies bind to target cells, like cancer cells, and signal natural killer (NK) cells to destroy them.

Antibodies can activate phagocytosis, where immune cells engulf and destroy target cells, by attaching to them and marking them for engulfment.

Therapeutic monoclonal antibodies can activate the complement system, a part of the immune system, leading to the lysis, or breakdown, of target cells.

Monoclonal antibodies, like Trastuzumab, can bind to receptors on cancer cells, blocking the growth factors that stimulate cell growth.

Monoclonal antibodies can induce internalization, where the target molecule on the cell surface is brought inside the cell, preventing it from signaling.

Monoclonal antibodies can be conjugated with bacterial toxins, which are poison-like substances, to specifically target and kill tumor cells.

Monoclonal antibodies can be conjugated with isotopes, which are atoms with different numbers of neutrons, for both imaging and therapeutic purposes.

Monoclonal antibodies can be designed to kill tumor cells without requiring internalization, meaning the antibody doesn't need to be taken into the cell to work.