Allergy And Hypersensitivity

An important undesirable side effect of immunity is the development, under some conditions, of allergy or other types of immune hypersensitivity. There are several types of allergy and other hypersensitivities, some of which occur only in people who have a specific allergic tendency.

Allergy Caused by Activated T Cells: Delayed-Reaction Allergy

Delayed-reaction allergy is caused by activated T cells and not by antibodies. In the case of poison ivy, the toxin of poison ivy in itself does not cause much harm to the tissues. However, on repeated exposure, it does cause the formation of activated helper and cytotoxic T cells. Then, after subsequent exposure to the poison ivy toxin, within a day or so, the activated T cells diffuse from the circulating blood in large numbers into the skin to respond to the poison ivy toxin. And, at the same time, these T cells elicit a cell-mediated type of immune reaction. Remembering that this type of immunity can cause release of many toxic substances from the activated T cells as well as extensive invasion of the tissues by macrophages along with their subsequent effects, one can well understand that the eventual result of some delayed-reaction allergies can be serious tissue damage. The damage normally occurs in the tissue area where the instigating antigen is present, such as in the skin in the case of poison ivy, or in the lungs to cause lung edema or asthmatic attacks in the case of some airborne antigens.

Allergies in the "Allergic" Person, Who Has Excess IgE Antibodies

Some people have an "allergic" tendency. Their allergies are called atopic allergies because they are caused by a nonordinary response of the immune system. The allergic tendency is genetically passed from parent to child and is characterized by the presence of large quantities of IgE antibodies in the blood. These antibodies are called reagins or sensitizing antibodies to distinguish them from the more common IgG antibodies. When an allergen (defined as an antigen that reacts specifically with a specific type of IgE reagin antibody) enters the body, an allergen-reagin reaction lakes place, and a subsequent allergic reaction occurs.

A special characteristic of the IgE antibodies (the reagins) is a strong propensity to attach to mast cells and basophils. Indeed, a single mast cell or basophil can bind as many as half a million molecules of IgE antibodies. Then, when an antigen (an allergen) that has multiple binding sites binds with several IgE antibodies that are already attached to a mast cell or basophil, this causes immediate change in the membrane of the mast cell or basophil, perhaps resulting from a physical effect of the antibody molecules to contort the cell membrane. At any rate, many of the mast cells and basophils rupture; others release special agents immediately or shortly thereafter, including his-tamine, protease, slow-reacting substance of anaphylaxis (which is a mixture of toxic leukotrienes), eosinophil chemotactic substance, neutrophil chemo-tactic substance, heparin, and platelet activating factors. These substances cause such effects as dilation of the local blood vessels; attraction of eosinophils and neu-trophils to the reactive site; increased permeability of the capillaries with loss of fluid into the tissues; and contraction of local smooth muscle cells. Therefore, several different tissue responses can occur, depending on the type of tissue in which the allergen-reagin reaction occurs. Among the different types of allergic reactions caused in this manner are the following.

Anaphylaxis. When a specific allergen is injected directly into the circulation, the allergen can react with basophils of the blood and mast cells in the tissues located immediately outside the small blood vessels if the basophils and mast cells have been sensitized by attachment of IgE reagins. Therefore, a widespread allergic reaction occurs throughout the vascular system and closely associated tissues. This is called anaphylaxis. Histamine is released into the circulation and causes body-wide vasodilation as well as increased permeability of the capillaries with resultant marked loss of plasma from the circulation. An occasional person who experiences this reaction dies of circulatory shock within a few minutes unless treated with epinephrine to oppose the effects of the histamine.

Also released from the activated basophils and mast cells is a mixture of leukotrienes called slow-reacting substance of anaphylaxis. These leukotrienes can cause spasm of the smooth muscle of the bronchioles, eliciting an asthma-like attack, sometimes causing death by suffocation.

Urticaria. Urticaria results from antigen entering specific skin areas and causing localized anaphylactoid reactions. Histamine released locally causes (1) vasodilation that induces an immediate red flare and (2) increased local permeability of the capillaries that leads to local circumscribed areas of swelling of the skin within another few minutes. The swellings are commonly called hives. Administration of antihista-mine drugs to a person before exposure will prevent the hives.

Hay Fever. In hay fever, the allergen-reagin reaction occurs in the nose. Histamine released in response to the reaction causes local intranasal vascular dilation, with resultant increased capillary pressure as well as increased capillary permeability. Both these effects cause rapid fluid leakage into the nasal cavities and into associated deeper tissues of the nose; and the nasal linings become swollen and secretory. Here again, use of antihistamine drugs can prevent this swelling reaction. But other products of the allergen-reagin reaction can still cause irritation of the nose, eliciting the typical sneezing syndrome.

Asthma. Asthma often occurs in the "allergic" type of person. In such a person, the allergen-reagin reaction occurs in the bronchioles of the lungs. Here, an important product released from the mast cells is believed to be the slow-reacting substance of anaphylaxis, which causes spasm of the bronchiolar smooth muscle. Consequently, the person has difficulty breathing until the reactive products of the allergic reaction have been removed. Administration of antihistaminics has less effect on the course of asthma because histamine does not appear to be the major factor eliciting the asthmatic reaction.


Abreu MT, Arditi M: Innate immunity and toll-like receptors: clinical implications of basic science research. J Pediatr 144(4):421, 2004.

Albert ML: Death-defying immunity: do apoptotic cells influence antigen processing and presentation? Nat Rev Immunol 4:223, 2004.

Alberts B, Johnson A, Lewis J, et al: Molecular Biology of the Cell. New York: Garland Science, 2002.

Cheroutre H, Madakamutil L: Acquired and natural memory T cells join forces at the mucosal front line. Nat Rev Immunol 4:290, 2004.

Cooper MA, Pommering TL, Koranyi K: Primary immunodeficiencies. Am Fam Physician 68:2001, 2003.

Cossart P, Sansonetti PJ: Bacterial invasion: the paradigms of enteroinvasive pathogens. Science 304:242, 2004.

Eisenbarth GS, Gottlieb PA: Autoimmune polyendocrine syndromes. N Engl J Med. 350:2068, 2004.

Figdor CG, de Vries IJ, Lesterhuis WJ, Melief CJ: Dendritic cell immunotherapy: mapping the way. Nat Med 10:475, 2004.

Frossi B, De Carli M, Pucillo C: The mast cell: an antenna of the microenvironment that directs the immune response. J Leukoc Biol 75:579, 2004.

Grossman Z, Min B, Meier-Schellersheim M, Paul WE: Concomitant regulation of T-cell activation and homeostasis. Nat Rev Immunol 4:387, 2004.

Kupper TS, Fuhlbrigge RC: Immune surveillance in the skin: mechanisms and clinical consequences. Nat Rev Immunol 4:211,2004.

La Cava A, Matarese G: The weight of leptin in immunity. Nat Rev Immunol 4:371, 2004.

Linton PJ, Dorshkind K: Age-related changes in lymphocyte development and function. Nat Immunol 5:133, 2004.

MacGlashan D Jr: Histamine: a mediator of inflammation. J Allergy Clin Immunol 112(4 Suppl):S53, 2003.

McGeady SJ: Immunocompetence and allergy. Pediatrics 113(4 Suppl):1107, 2004.

Nikolich-Zugich J, Slifka MK, Messaoudi I: The many important facets of T-cell repertoire diversity. Nat Rev Immunol 4:123, 2004 .

Petrie HT: Cell migration and the control of post-natal T-cell lymphopoiesis in the thymus. Nat Rev Immunol 3:859, 2003.

Scott CC, Botelho RJ, Grinstein S: Phagosome maturation: a few bugs in the system. J Membr Biol 193:137, 2003.

Theoharides TC, Cochrane DE: Critical role of mast cells in inflammatory diseases and the effect of acute stress. J Neu-roimmunol 146:1, 2004.

Vivier E, Anfossi N: Inhibitory NK-cell receptors on T cells: witness of the past, actors of the future. Nat Rev Immunol 4:190, 2004.

51 Ways to Reduce Allergies

51 Ways to Reduce Allergies

Do you hate the spring? Do you run at the site of a dog or cat? Do you carry around tissues wherever you go? Youre not alone. 51 Ways to Reduce Allergies can help. Find all these tips and more Start putting those tissues away. Get Your Copy Of 51 Ways to Reduce Allergies Today.

Get My Free Ebook


  • Habte
    What is allergin reagin reaction occurs in bronchioles of the lungs?
    3 years ago
    What is allergen reagin reaction called?
    3 years ago
  • derek gibson
    What is the allergn reagin reaction that occurs in bronchioles called?
    10 months ago

Post a comment