Hypersensitivity may be stated as the procedure in which adaptive immune response becomes over sensitive to the diversity of infectious and innocuous antigens thus inflicting injury to host tissue. Disorders which result from such reactions are termed hypersensitivity diseases.
The most significant function of adaptive immune response is in host defense against microbes. Though, it could also be liable for tissue injury and disease. This reaction could generate discomfort and at times may result in fatality.
Kinds of Hypersensitivity Reactions:
There are 5 kinds referred to as Type I, II, III, IV and V. Once contact is established with antigen a variation in timing exists for each of hypersensitivity reactions
i) Type 1 hypersensitivity reaction: which is allergy affects approx 17% of population and it exists in 2 phases and mediated by IgE. It is the immediate hypersensitivity reaction as antibodies are involved and begins within minutes of contact with antigen. Mechanism of action comprises mast cells and basophils, both of which contain receptors for IgE.
ii) Hypersensitivity Type II reaction: also known as cytotoxic reaction comprises IgE and IgM antibodies. These antibodies interact with antigen in blood and analogous antigens on surface of human body cells. This is achieved by opsonization and phagocytosis of cells. Such mechanisms set off complement system which lyses the cell.
iii) Hypersensitivity type III: mobilizes not only IgE and IgM but also immune complexes. It can rise from soluble antigens. Immune complexes could differ in size, amount, affinity and isotype of responding antibody. As a result, large immune complexes fix complements and are disposed by mononuclear phagocytes from circulation, while smaller complexes deposit in blood vessel walls and can ligate Fc receptors on mast cells and other leucocytes that can lead to leucocyte activation and tissue injury.
iv) Type IV hypersensitivity: known as delayed type hypersensitivity (DTH) reaction takes place inside 24-72 hours and it is mediated by CD4, CD8 T cells and antigen peptide cells (APCs) e.g. Langerhans' cells. Activated T cells migrate to site of antigenic entry where pro-inflammatory mediators like Tumor necrosis factor (TNF) are released.
v) Stimulatory or type V: hypersensitivity are mediated by auto-antibodies. It is categorized as the distinct kinds of hypersensitivity where auto-antibodies bind to hormone receptors which imitate hormone itself and this leads to stimulation of target cells. Autoimmune response states ability of the individual immune system to react with self antigens.
Diseases Associated With Hypersensitivity Reactions:
Hypersensitivity diseases are clinically heterogeneous group of disorders whose manifestations are stated by kind of immune response which leads to cell and tissue injury. Mechanisms of immune response which leads to different kinds of hypersensitivity reactions have been defined above. There are some individuals prone to generate IgE in response to environmental allergens and illustrate strong immediate hypersensitivity are said to be atopic and they undergo from allergy. This form of allergy may present in different forms like hay fever, asthma, urticaria (hives) or chronic skin irritation. In extreme cases called as anaphylaxis, mast cell and basophil derived mediators limit airways to point of asphyxiation and generate cardiovascular collapse leading to death.
Introduction to Immunopathology:
Immunopathology is branch of immunology which deals with pathologies of immune system. It can also be explained as branch of medicine which deals with immune responses related with diseases. Immune system assists fight off infections but could also turn around to be harmful because of over activity and which is immunopathology. Though, with deeper understanding of pathogenesis of some diseases like tuberculosis and leprosy and growth of experimental models of some diseases such as Masugi nephritis, and lymphocytic choriomeningities immunopathology was then viewed in the wider context of immunologic event.
Pathology of Immune Response:
When the reaction is useful, there are no signs or symptoms on affected person, and lifelong immunity is conferred on individual. The role performed effectively by Adaptive immune response. If effect on patient is neutral, the individual experience symptoms, as a result of the response of the immune system to infections, primarily cytokines released from phagocytes and toxins released from dying bacteria. Cytokines influence the local blood vessels, causing inflammation; redness and swelling of skin. Cytokines also play the important role in adhesive properties of endothelium, causing circulating leukocytes to attach to endothelial cells of blood vessel wall and migrate between them to the site of infection, to which they are attracted by other cytokines. This action accounts for the pain experienced during infection. The length or duration of immunopathological symptoms relies upon nature of infection and defense system of affected person. Though, this doesn't mean that the rise in intensity of symptoms is the indication of advancement in infection or disease, but in most cases recommends that immune response system is effective in combating infectious pathogens like diarrhea and vomiting related with food poisoning are fairly essential in eliminating harmful toxins.
Antibodies are generated only in response to particular infections, therefore antibodies present in the individual directly represents number of pathogens the individual has been exposed to. Adaptive immune responses depend on activities of lymphocytes. Lymphocytes assist to recognize and defend against pathogenic molecules not recognized by phagocytes and macrophages like Viruses and bacteria with protective capsules. Mature dendritic cells are found extensively in T-cell.
Immunopathology of Infectious Diseases:
Immunopathology captures both hypersensitivity and autoimmunity as a result of overactive immune system and immunodifficiency that is the incapability of the individual to fight infection. If the virus infects the host, immune response is produced that could find out survival or death of host in case of acute infection or persistent/chronic infection. This kind of infection could result in tissue damage or pathology and it is dissimilar from direct virus attack on cells resulting in tissue damage or apoptosis. Therefore there should be balance between viral clearance and immunopathology.
Immunopathology of Parasites:
Tissue damaging reactions take place when there is constant infection of parasites like Plasmodium malariae, Schistosomajaponicum. This is due to persistence of parasite antigen in blood leads to immunopathological disorders like immune complex nephrotic syndrome, liver granuloma and autoimmune lesions of heart. It is thought that cross reactions between parasite and self could result in autoimmunity and is basis for cardiomyopathy in Chagas disease. Generalized immunosupression increases vulnerability to bacterial and viral infections.
Diseases of the Blood:
There are some immunological diseases called as cytopenia are blood diseases e.g. autoimmune neutropenia, immune thrombocytopenic purpura etc. These are thought to be autoimmune diseases caused by destruction of blood components by autoantibodies.
Auto-immunology and auto-pathology:
While Auto-immunology is branch of immunology which deals with Autoimmunity, Auto-pathology is pathology which explainsthe autoimmune system. Immune system of the individual is well prepared to protect it against invasion by dangerous microorganisms, but at times immune system fails to recognize its own constituent parts, thus attacking its own cells and tissues. This procedure of permitting immune responses against itself is known as Autoimmunity.
Possible Causes of Autoimmunity:
Adaptive immune responses are liable for autoimmunity, and its actions are like the way it acts against foreign antigens. Though, in case of self antigens, it is approximately not possible for immune response mechanism to eradicate antigen entirely, thus prolonging response that could be detrimental to affected tissues in most cases. There is no particular explanation to why adaptive immune response attacks its own self; rather vulnerability to autoimmune diseases appears to be caused by the combination of factors; genetics, sex and environment.
i) Genetic factors:
Certain individuals who have family or personal history of autoimmune diseases are probable to be vulnerable to autoimmunity. This vulnerability is discovered to be related with combination or group of genes. Based on twin and family studies performed for numerous autoimmune diseases like insulin-dependent diabetes mellitus, genes associated to immunoglobulins, T-cell receptors, and major histocompatibility complexes (MHC) have been suspected to be chiefly liable for autoimmunity. Though, the most constant association for susceptibility to autoimmunity has been related to MHC genotype. Genes associated to immunoglobulins and T-cell receptors, involved in antigen recognition, are essentially variable and vulnerable to recombination. This quality allows immune system to respond to the broad variety of harmful pathogens, and thus give rise to lymphocytes capable of self- immunity.
It has been seen that frequency of autoimmune diseases is higher in females than males, though studies also demonstrate that autoimmune diseases present in males tend to be harsh. Though, the reasons for this anomaly are uncertain, but there are some descriptions to wide range in frequency between two sexes. Compared to males, females show larger inflammatory responses, when their immune system is triggered, therefore increasing risk of autoimmunity.
iii) Environmental Factors:
Different studies have illustrated that expression of the disease could be affected by environmental factors. As presence of the autoantibody need the autoantigen to cause autoimmunity, definite factors have been seen to inhibit or influence binding of autoantibody to the autoantigen, thus modulating expression of the diseases among different individuals. For instance, in Goodpasture's disease, it was seen that cigarette smokers completely shown pulmonary haemorrhage where as non cigarette smokers exhibited no sign of pulmonary haemorrhage. Different hypotheses have attempted to describe this correlation, but details of mechanism aren't fully known. Certain chemicals and drugs have also been implicated in expression of autoimmunity like in drug- induced lupus erythematosus; withdrawal of the drug removes the symptoms automatically.
Pathology of Autoimmunity:
Pathology and clinical expression of the autoimmune disease is determined by antigens or group of antigens, together with method by which the antigen-bearing tissue is injured. Antigens liable for autoimmunity are known to be few in number (DNA, receptor), and numerous have been seen to play signaling roles in immune response, whereas the mechanisms operative in pathology of the autoimmune disease are numerous, and are generally mediated by actions of autoantibodies and T cells. Tissue damage can also be because of the binding of autoantibodies to autoantigens in extracellular matrix or binding of autoantibodies to soluble autoantigens. T cell responses have been directly implicated in causing tissue damage or indirectly by activation of macrophages. It was seen in autoimmune disease insulin-dependent diabetes mellitus, which especially reactive T cells selectively destroyed insulin-producing β cells of the pancreatic islets. Molecular mimicry, significant mechanism discovered to be significant in autoimmunity, involves production of antibodies to the antigen which mimics the self antigen, thus causing binding of antibodies to the self antigens.
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