What Is Immunopathology?

Immunopathology is the science that studies pathological phenomena caused by dysfunction (or secondary abnormalities) and immune responses.

Immunopathology

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Immunopathology is the science that studies pathological phenomena caused by dysfunction (or secondary abnormalities) and immune responses.
Chinese name
Immunopathology
Foreign name
immunopathology
Pinyin
mianyi binglixue
Including
Autoimmunity, immune proliferation, and immunodeficiency
mianyi binglixue
Immunopathology
immunopathology
It is one of the branches of immunology, covering a wide range, including (allergic reactions), autoimmunity, immune proliferation, and immune deficiency. Although the immune system recognizes and rejects antigenic foreign bodies, it is beneficial to the body in most cases, but there are also some immune reactions that are not good for the body and can cause dysfunction or (and) tissue damage, such as rejection of grafts and self-components Immune response.
When hyperproliferative occurs, a primary pathological process occurs, namely an immunoproliferative disease. Normal (reactive) immune hyperplasia can be self-limiting and recover over a course of illness. Malignant immune hyperplasia, how to treat Jackin's disease, macroglobulinemia, heavy chain disease, multiple myeloma, etc. Multiple myeloma is a disease characterized by massive proliferation of plasma cells, affecting the bone, bone marrow, kidney, and nervous system. The vast majority of patients only have a sexual change in a cloned B cell, and an abnormal immunoglobulin with unknown antibody activity, that is, bone marrow globulin.
The body reduces or loses normal immune function due to some reason of the immune system. Immune deficiency can be primary (caused by genetic or congenital causes) or acquired (caused by other diseases). Immunodeficiency can also be divided into humoral immunodeficiency and cellular immunodeficiency.
Primary immunodeficiency is hereditary, such as sexual interlocking or autosomal inheritance; congenital, such as embryonic dysplasia, resulting in the loss of a certain tissue component or an abnormal enzyme system. Common types are: Immunoglobulin (Ig) defects: some patients are deficient or low in various types of Ig, and some patients have only one or several types of Ig defects, while others are normal. The most common of these is selective IgA deficiency, with one in every 500 to 700 people. The common symptom is the recurrence of severe bacterial infections. The main cause of Ig defects is abnormal B cell systems, but there are also suppressive T cells in some cases. Hyperfunction causes B-cell function to be inhibited; Cell immune deficiency: a disease caused by abnormal development of the thymus. Typical examples are DiGeorge syndrome and Nezelov syndrome. The former is due to congenital dysplasia, and the latter is due to thymic hypoplasia. Mainly manifested by multiple intracellular parasitic bacterial and fungal infections and viral infections, DiGeorge syndrome is also accompanied by abnormalities of the parathyroid glands and the cardiovascular system; combined immunodeficiency: lack of humoral immunity and lack of cellular immunity.
In addition to the appropriate selection of antibiotics for the treatment of relevant infections, Ig should be supplemented for humoral immunodeficiency. For cellular immunodeficiency, fetal thymus and fetal liver can be transplanted to provide stem cells or thymosin can be injected. Bone marrow transplantation can also be considered.

Immunopathology transplant immunity

The study of post-transplant rejection has its origins in studies of histocompatibility antigens in humans and mice. The presence of this antigen on white blood cells makes tissue matching possible, thus creating conditions for selecting a reliable donor before organ transplantation. At the same time, attention has been paid to the relationship between certain HLA phenotypes and diseases (especially immune diseases) in humans, and some progress has been made.
The progress in transplantation immunity can be largely attributed to the establishment of pure-line animals, especially mouse pure-line animals, and on the basis of this, breeding homologous mice. The study of these animals not only enriches the immune genetic content of mice, but also provides a reference for understanding the genetic laws of histocompatibility in humans, making a great contribution.
In addition, a large number of studies have been conducted on immune non-reactivity or immune tolerance, and they have been coordinated with the research on immunity. The experiments of Billingham, Brent, and Medawar have proven that the importation of adult animal cells in embryonic or neonatal mice can Induces specific transplant tolerance. The central idea of this experiment is based on Brunet's cell clone selection theory, and it is also the theoretical starting point of the host anti-graft response (HVGR). On this basis, another opposite phenomenon, namely the graft-versus-host response (OVHR), has attracted attention, and research has begun to provide conditions for the success of postoperative mid-medium bone marrow transplantation.
In the 1980s, monoclonal antibody and cell cloning techniques that distinguished T cell subgroups were used to analyze the cellular basis of participation in acute graft rejection, and achieved good results in improving graft survival. For example, the treatment of donor bone marrow cells with monoclonal antibodies in recent years has greatly improved the survival rate of bone marrow transplantation.

Tumor immunology

Through tumor immunity and research on immunochemical analysis of human and animal tumors and leukemia cells, several important issues have been clarified, such as the lack of various normal tissue components of tumor cells and the reproduction of certain antigens that normally exist in the embryonic stage; in some tumors New antigens (neoantigen) appear. The emergence of tumor neoantigens indicates that tumor cells have acquired new genetic information, and may also be caused by the introduction of virus genomes into cells.

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