Publications by authors named "Tatyana Khramova"

Thyroglobulin is a major autoantigen to which autoimmune response, destroying the thyroid gland in Hashimoto's thyroiditis, is directed. To detect a pathological autoimmune response to thyroglobulin, as well as the successful induction of experimental autoimmune thyroiditis, thyroglobulin carrying thyroiditogenic epitopes is necessary. It is not known which features of thyroglobulin structure determine the presence of thyroiditogenic epitopes and can serve as markers of their presence.

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Background: We have earlier discovered a new factor of autoimmunity downregulation, called regulatory rheumatoid factor (regRF). Being anti-idiotypic antibodies, regRF restricts the expansion of CD4 T lymphocytes to the idiotype of which it is specific, according to the negative feedback principle. It has been shown that only activated CD4 T lymphocytes are the target of regRF.

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Article Synopsis
  • The AIDS autoimmune hypothesis suggests that managing autoimmunity against CD4 T lymphocytes could improve HIV infection outcomes.
  • The study explores using neonatal immunization with gp120 to prevent the harmful autoimmune response against CD4 lymphocytes initiated by HIV-1.
  • Results from both computer modeling and experimental studies indicate that neonatal immunization can suppress the production of anti-CD4 autoantibodies, promoting tolerance to CD4 and preventing autoimmune issues in adult rats triggered by gp120.
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Background: Previously, we identified a regulatory rheumatoid factor (regRF), the production of which provides rats with resistance to collagen-induced arthritis (CIA). Immunization with conformers of IgG Fc fragments carrying epitopes specific to regRF reduces symptoms of CIA. The aim of this study was to determine whether there is a link between regRF levels and rheumatoid arthritis (RA) activity in humans in order to assess the potential of regRF as a therapeutic biotarget in RA.

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Previously we identified a rheumatoid factor, the production of which provides rats with resistance to experimental autoimmune diseases. It has been named regulatory rheumatoid factor (regRF). Immunization with conformers of IgG Fc fragments carrying epitopes specific to regRF reduces rat collagen-induced arthritis.

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Introduction: A high level of total cholesterol or low-density lipoprotein (LDL) cholesterol is considered the main cause of atherosclerosis and cardiovascular disease. For this reason, experimental atherosclerosis is induced by creating high blood cholesterol in animals. However, the hypothesis that atherosclerotic processes are mostly caused by immune (autoimmune) mechanisms has recently been gaining traction.

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Immunoglobulin G can inhibit antibody response. The mechanism of immunosuppression by immunoglobulins remains unknown. Recently, we found a new factor of immunoregulation referred to as regulatory rheumatoid factor (regRF).

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Article Synopsis
  • The study explores how regulatory rheumatoid factor (regRF) can prevent autoimmunity by limiting lymphocyte expansion during immune responses.
  • Experimental models showed that rats producing regRF had fewer CD4+ lymphocytes after immunization with myelin basic protein (MBP) compared to those with lower regRF levels.
  • Findings suggest that regRF specifically targets and helps control antigen-activated CD4+ lymphocytes, indicating its potential role in autoimmunity regulation.
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Article Synopsis
  • The study investigates how anti-CD4 autoantibodies and rheumatoid factor (RF) contribute to CD4 lymphocyte loss in HIV-infected individuals, particularly focusing on how uninfected cells die.
  • Immunization of Wistar rats with HIV-1 gp120 leads to increased anti-CD4 autoantibodies and decreased CD4 cell counts, although the autoantibodies don't kill the cells directly.
  • The study concludes that the combined effects of anti-CD4 autoantibodies and RF are necessary for the death of CD4 lymphocytes, suggesting a potential mechanism that could also apply to HIV-infected humans.
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The regulation of autoimmunity is a key issue in fundamental immunology. Despite outstanding achievements on this front, we currently have more questions than answers. The idea of an immune network as a regulatory mechanism is quite attractive, since it enables us to explain the selectivity (specificity), and moreover the clonality, of the regulation.

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