Types of Hypersensitivity

The body’s immunity recognizes foreign antigens and responds by producing antibodies against them. However, sometimes the body acts on a foreign antigen or stimulus is in an exaggerated manner, whose results can be harmful to the body. Therefore, hypersensitivity is an exaggerated immune reaction by the body to a foreign antigen. Examples include anaphylaxis and allergic reactions. The condition may also involve the reaction of the body against self-antigens when mechanisms of self-tolerance fail, a condition which results in autoimmune disorders which manifest as chronic disorders.

Pathophysiology

The body is exposed to the foreign antigens through the skin, the digestive tract or the respiratory system. The immune system recognizes these antigens; they are then degraded into smaller proportions. Later, they are presented on the surface of antigen-presenting cells (APCs) where they wait to be recognized by the T cells that are specific to the antigen (s) in question. The Th2 cells induced produce IL-5, IL-4, and IL-10 cytokines. An interaction between the Th2 cells and B cells then results in the activation of the B cells. Th2 cytokine and IL-4 makes the B cells to start producing IgE instead of IgM antibodies. IgE antibodies have mast cells and basophils receptors on their surfaces. The interaction results in the production of leukotriene, histamine, and prostaglandin all of which are responsible for the development of the symptoms of allergic reactions.

Types of hypersensitivity

There are four types of hypersensitivity namely; type I (immediate hypersensitivity reactions), type II (cytotoxic hypersensitivity reactions), type III (complex immune reactions) and type IV (delayed hypersensitivity reactions). In type I hypersensitivity reaction, the response to the foreign antigen is very fast, about 30 minutes. Exposure to the allergen can be through injection, direct contact, inhalation, and ingestion. The common ones are pollen, some drugs and chemical additives, certain foods and insect stings. Once the Th2 cells are presented with the antigens; they trigger the production of IgE antibodies which have receptors for mast cells and basophils. After binding, they produce the vasoactive amines and histamine which are responsible for the signs and symptoms of allergic reactions. When it is severe, anaphylactic shock occurs. The patient suffers from breathing difficulties, low blood pressure and can even die. However, the effects can be reversed by epinephrine injections (Hou 1-12).

Type II hypersensitivity reactions depend on antibody-mediated responses. The antigen found on the membrane of the cell attracts the specific antibody which upon binding can destroy the entire cell. It mainly targets the cells instead of the pathogens. The antibodies surround the cell whose layer contains the antigen of interest by a process called opsonization. They do this by fixing the complement system through the classical pathway, phagocytosis or by apoptosis. The complement system activates the membrane attack complex (MAC) which causes cell lysis. The antibodies majorly doing this are IgM and IgG. The diseases found under this type include; autoimmune hemolytic anemia, erythroblastosis fetalis and good pasture’s syndrome (Beenhouer 209-304).

Type III hypersensitivity reactions result in tissue damage, caused by immune complexes. Sometimes, it happens that the body is not clearing the antigens effectively. Thus, it results in a high number of antigens as well as antibodies in the body. You will find that a single antibody is bound to several antigens and a single antigen could be attached to several antibodies. Therefore, clumps containing antibodies and antigens are formed. These clusters then deposit in the tissues of kidneys or joints, causing inflammation. The response time is slower than that found in type I hypersensitivity reactions. They develop about 3 to 6 hours after antigen exposure. The reactions activate complement and also attract neutrophils. Some of the diseases include lupus, rheumatoid arthritis and post strep glomerulonephritis (Delves).

Type IV hypersensitivity reactions happen 48-72 hours of antigen exposure. Unlike the other responses which were mediated by antibodies, these are mediated by T cells and macrophages/monocytes. They majorly target intracellular pathogens such as fungi, parasites, and mycobacteria. Once the antigen enters the body, monocytes accumulate at that site. The antigen is taken up by the monocyte or macrophage, processed and presented to the cytotoxic T cells. A macrophage and a T cell form an infiltrate known as granuloma in the tissues. It also occurs in transplant rejected tissues and organs and even in tumors. Examples include; contact dermatitis and multiple sclerosis. Patients who have HIV/AIDS typically have low CD4+ cells count. As such, their bodies are usually unable to kill the intracellular pathogens because the T cells are unable to recognize them. Therefore, the pathogens remain in the macrophages. HIV/AIDS patients are hence, susceptible to the opportunistic diseases such as tuberculosis. Most AIDS patients die from these opportunistic infections because their bodies are unable to kill these intracellular pathogens.

Works Cited

Beenhouer, D. ""Chapter 17 – Molecular Basis of Diseases of Immunity."" Molecular Pathology (2009): 209-304.

Delves, J. Peter. ""Drug Hypersensitivity."" 08 Sep 2017. MSDManuals. 13 Dec 2017.

Hou, W. ""CHAPTER 1 – Basic immunology and immune system disorders."" Treating Autoimmune Disease With Chinese Medicine (2011): 1-12.