Hypersensitivities
Maladaptive immune responses toward harmless foreign substances or self antigens that occur after tissue sensitization are termed hypersensitivities. This can potentially be very dangerous for an individual, as the immune response can be very powerful; it can destroy host tissue if not kept in check. The types of hypersensitivities include immediate, delayed, and autoimmunity hypersensitivities. A large proportion of the population is affected by one or more types of hypersensitivity.
Allergies
The immune reaction that results from immediate hypersensitivities, in which an antibody-mediated immune response occurs within minutes of exposure to a harmless antigen, is called an allergy. In the United States, 20 percent of the population exhibits symptoms of allergy or asthma, whereas 55 percent test positive against one or more allergens. Upon initial exposure to a potential allergen, an allergic individual synthesizes antibodies of the IgE class; this class of antibodies also mediates the immune response to parasitic worms. The constant domain of the IgE molecules interacts with mast cells embedded in connective tissues. This process primes, or sensitizes, the tissue. Upon subsequent exposure to the same allergen, IgE molecules on mast cells bind the antigen via their variable domains, stimulating the mast cell to release the modified amino acids histamine and serotonin. These chemical mediators then recruit eosinophils which mediate allergic responses . The effects of an allergic reaction range from mild symptoms such as sneezing and itchy, watery eyes, to more severe or even life-threatening reactions involving intensely-itchy welts known as hives, airway contraction with severe respiratory distress, and plummeting blood pressure. This extreme reaction is known as anaphylactic shock. If not treated with epinephrine to counter the blood pressure and breathing effects, this condition can be fatal.
Allergens
This image shows an example of an allergic response to ragweed pollen. On first exposure to an allergen, an IgE antibody is synthesized by plasma cells in response to a harmless antigen. The IgE molecules bind to mast cells. On secondary exposure, the mast cells release histamines and other modulators that affect the symptoms of allergy.
Delayed hypersensitivity is a cell-mediated immune response that takes approximately one to two days after secondary exposure for a maximal reaction to be observed. This type of hypersensitivity involves the TH1 cytokine-mediated inflammatory response. It may manifest as local tissue lesions or contact dermatitis (rash or skin irritation). Delayed hypersensitivity occurs in some individuals in response to contact with certain types of jewelry or cosmetics. It also facilitates the immune response to poison ivy and is the reason why the skin test for tuberculosis results in a small region of inflammation on individuals who were previously exposed to Mycobacterium tuberculosis. Cortisone is typically used to treat such responses as it inhibits cytokine production.
Autoimmunity
Autoimmunity is a type of hypersensitivity to self antigens that affects approximately five percent of the population. Most types of autoimmunity involve the humoral immune response. Antibodies that inappropriately mark self components as foreign are termed autoantibodies. In patients with the autoimmune disease myasthenia gravis, muscle cell receptors that induce contraction in response to acetylcholine are targeted by antibodies. The result is muscle weakness that may include marked difficultly with fine and/or gross motor functions. In systemic lupus erythematosus, a diffuse autoantibody response to the individual's own DNA and proteins results in various systemic diseases. Systemic lupus erythematosus may affect the heart, joints, lungs, skin, kidneys, central nervous system, or other tissues, causing tissue damage via antibody binding, complement recruitment, lysis, and inflammation .
SLE and autoimmunity
Systemic lupus erythematosus is characterized by autoimmunity to the individual's own DNA and/or proteins, which leads to varied dysfunction of the organs.
Autoimmunity can develop with time; its causes may be rooted in molecular mimicry. Antibodies and TCRs may bind self antigens that are structurally similar to pathogen antigens, which the immune receptors first raised. As an example, infection with Streptococcus pyogenes (bacterium that causes strep throat) may generate antibodies or T cells that react with heart muscle, which has a similar structure to the surface of S. pyogenes. These antibodies can damage heart muscle with autoimmune attacks, leading to rheumatic fever. Insulin-dependent (Type 1) diabetes mellitus arises from a destructive inflammatory TH1 response against insulin-producing cells of the pancreas. Patients with this autoimmunity must be injected with insulin that originates from other sources.