Recovery from autoimmunity of MRL/lpr mice after infection with an interleukin-2/vaccinia recombinant virus

Article Abstract:

The cytokine interleukin-2 (IL-2) is made by T lymphocytes and is involved in the maturation and expansion of T lymphocytes that are activated by antigen, molecules that are recognized by the immune system as foreign. Il-2 is also thought to be involved in autoimmune disease. The MRL/lpr strain of mice, which develops systemic lupus erythematosus (SLE) early in life, serves as an animal model for human SLE. The MRL/lpr mice develop symptoms of autoimmune diseases such as glomerulonephritis (inflammation of the glomerulus of the kidneys due to the presence of immune complexes), arthritis, and arteritis (inflammation of the arteries). Associated with the autoimmune disease are abnormalities of the immune system including atrophy of the thymus and enlargement of the lymph nodes due to the abnormal proliferation of a certain subset of immature T lymphocytes. The effect of IL-2 on the progression of the autoimmune disease was examined in the mice. IL-2 was introduced to the mice by vaccination with a vaccinia virus that had been genetically engineered to express IL-2. The mice that were vaccinated survived longer than unvaccinated mice, and had decreased levels of autoantibodies and rheumatoid factor. They did not have lymphocytes infiltrating the kidneys. The glomerulus of the kidneys did not contain cells that were multiplying abnormally, and their joints were cleared of immune cells. With IL-2 treatment, the thymocytes differentiated normally and the subset of lymphocytes that were increased in the disease state were reduced. Normal numbers of mature lymphocytes were found in the lymph nodes. Therefore, the introduction of IL-2, via vaccination with a recombinant vaccinia virus that expresses IL-2, causes the maturation of cells in the immune system that cannot mature normally in autoimmune disease. Treatment with Il-2 cleared the symptoms of autoimmune disease that occurred in the kidneys and joints. IL-2 can potentially be developed as a treatment for autoimmune diseases, such as systemic lupus erythematosus and rheumatoid arthritis in humans, and for acquired immunodeficiency syndrome (AIDS), where there is also a deficiency of IL-2 and increased numbers of immature T lymphocytes. (Consumer Summary produced by Reliance Medical Information, Inc.)

Models, Rheumatoid arthritis, Systemic lupus erythematosus, Cell differentiation, T cells, Interleukin-2

---

T-cell recognition of an immunodominant myelin basic protein epitope in multiple sclerosis

Article Abstract:

Multiple sclerosis (MS) is a progressive degenerative disease that involves the removal of the sheath of the protein myelin surrounding nerve fibers. It is an autoimmune disease, meaning that normal body components are reacted against by the immune system. The disease is thought to be due to the reactivity of T lymphocytes (white blood cells of the immune system) with myelin, as patients with MS have in their blood T cells that are reactive to myelin. Patients with MS often have particular types of histocompatibility class II antigens, DR2 and DQw1. Histocompatibility antigens are cell surface proteins that form complexes with antigens. Histocompatibility antigens are necessary for immune cells to recognize antigens, to determine if they are foreign or self and for a proper immune response to be mounted. T cells from 15,824 patients with MS, other neurological diseases, or from normal patients as controls, were grown in tissue culture. A greater number of T cells from patients with MS were reactive with a particular region of the myelin protein that formed a complex with DR2. Similar numbers of T cells from MS patients and from control subjects reacted with another region of the myelin protein that formed a complex with the histocompatibility antigen DRw11. Therefore the region that is recognized with DR2 and is reactive only in patients with MS appears to be the important region of the myelin protein that is recognized in MS. By understanding what region of the myelin protein is recognized, the course of disease can potentially be changed by altering the immune system so that this region is not recognized. This could theoretically be done by eliminating the T cells that recognize this region of the myelin protein or by inducing tolerance, so that the region would not be recognized as foreign. (Consumer Summary produced by Reliance Medical Information, Inc.)

Multiple sclerosis, Protein research, HLA class II antigens, Myelin sheath

---

Progression of autoimmune diabetes driven by avidity maturation of a T-cell population

Article Abstract:

Research is presented into the pathogenesis of autoimmune diabetes driven by the avidity maturation of a pancreatic beta-cell-specific T-lymphocyte population.

Type 1 diabetes

Similar abstracts:

• Abstracts: Self-similarity of extinction statistics in the fossil record. Fossil fish up for election
• Abstracts: Possible flush instability in mantle convection at the Archaean-Proterozoic transition. The realms of Archaean life
• Abstracts: Developmental and activity-dependent regulation of kainate receptors at thalamocortical synapses. Identification of genes that modify ataxin-1-induced neurodegeneration
• Abstracts: Female preference for specific pulse duration of male songs in the grasshopper, Omocestus viridulus. Use and function of genital contacts among female bonobos
• Abstracts: Imaging circumstellar environments with a nulling interferometer. Interferometric radar measurements of water level changes on the Amazon flood plain

This website is not affiliated with document authors or copyright owners. This page is provided for informational purposes only. Unintentional errors are possible.