hypersensitivityrefers to extreme physical sensitivity to certain substances or conditions. It is the unwanted reactions that the normal immune system produces in the form of allergies and autoimmunity. In other words, it is an overreaction of the immune system, and these reactions can be harmful, uncomfortable, or occasionally fatal. You can classify hypersensitivity into five types based on their mechanism and of course the time the reaction lasts.

  • type I hypersensitivity,
  • type II hypersensitivity,
  • then type III hypersensitivity,
  • Type IV hypersensitivity
  • and finally Type V hypersensitivity.

Type I, II and III areantibody-mediatedHypersensitivity (immediate), while Type IV is a cell-mediated (delayed) hypersensitivity reaction.

contents hide


1.1 1. Anaphylaxis

1.1.1 Immediate Phase

1.1.2 Late Phase

1.2 2. Atopy

1.3 Symptoms

1.3.1 Tempo

1.5 Treatment


2.1 Examples

2.2 Symptoms

2.3 Treatment


3.1 Examples

3.2 Symptoms

3.2.1 Tempo

3.3 Treatment


4.1 1. Contact hypersensitivity

4.2 2. Tuberculin-like hypersensitivity reaction

5 symptoms

6 Diagnose




A type I hypersensitivity reaction is commonly referred to as an allergic or immediate hypersensitivity reaction. This reaction is always rapid and can occur within minutes of exposure to an antigen. Type I hypersensitivity reactions are triggered by interactions between an IgE antibody and a multivalent antigen.

(IgE antibodies are a class of antibodies produced in allergic reactions, and multivalent antigen is an antigen molecule with more than one identical epitope per molecule)

Type I hypersensitivity reactions can be induced by a special type of antigen called an antigenAllergenswhich has all the characters ofnormalhumorous answer. Thus, an allergen induces a humoral antibody response, resulting in the production ofantibody secretionplasma cells and storage cells.

Common allergens for type I hypersensitivity are plant pollen, foods (nuts, eggs, shellfish, etc.), certain medications (penicillin, salicylates, local anesthetics, dust mites, etc.)

The Type I reaction can occur in two ways:

  • Anaphylaxie u
  • Atopy

The exact component of why some people are more prone to type 1 hypersensitivity is unclear. However, it has been shown that these individuals preferentially produce more lymphocytes or TH2 cells, which in turn favors class switching.For megE.

1. Anaphylaxis

It is an acute and potentially fatal immediate-type hypersensitivity reaction. The timing of onset of symptoms depends on the degree of hypersensitivity and location of exposure to the antigen. It usually affects the skin, respiratory tract, and cardiovascular system. Plasma cells secrete IgE in response to allergen-specific TH4 cells. This class of antibodies binds with high affinity to the Fc receptor on the surface of mast cells and tissue basophils. The binding of IgE to mast cells is also referred to asawareness.IgE-coated mast cells can become activated after repeated exposure to antigens. The main cellular components in this hypersensitivity are mast cells, eosinophils and basophils.


More. Anaphylaxis has two stages:

  • right away
  • Abend

immediate stage

This phase is characterized by degranulation and release of pharmacologically active mediators minutes after re-exposure to the same antigen. Histamine is the main biogenic amine causing rapid vascular and smooth muscle responses.

late stage

This phase begins to develop 4 to 6 hours after the immediate phase reaction and may last 1 to 2 days. It is identified by infiltration of neutrophils, macrophages, eosinophils, and lymphocytes at the reaction site.

2. Atopy

In contrast to anaphylaxis, atopy is a periodic, non-fatal, immediate hypersensitivity reaction. Atopic people produce higher levels of IgE in response to allergens than normal people who don't. An example of atopic reactions is bronchial asthma. Atopic hypersensitivity is not transmitted by lymphoid cells but can be transmitted by serum.


Some of the most common symptoms are skin rashes, tingling around the mouth, diarrhea, etc. It can affect many organs in the body including the skin (urticaria and eczema), the eyes (conjunctivitis), and the nose (rhinorrhea).


It usually takes 10 to 30 minutes for symptoms to appear, and sometimes it can take 10 to 12 hours.


Your diagnosis may include skin tests such as prick and intradermal tests. In addition, IgE and total IgE antibodies specific to the suspected allergens were measured.


Antihistaminesare used to treat type I hypersensitivity reactions. These drugs block histamine receptors on the surfaces of cell membranes.

Anaphylactic symptoms are treated with injectionsAdrenalin, a powerful neurotransmitter and hormone that effectively suppresses the immune response.

IgG-BlockerThey are also used to treat type I hypersensitivity.


Type II hypersensitivity is also known ascytotoxichypersensitivity orantibody-mediatedhypersensitivity reactions. In addition, it can affect a variety of organs and tissues. Type II hypersensitivity reactions involve antibody-mediated destruction of cells by immunoglobulin classes of heavy chains other than IgE.

Also see:Classes and structure of immunoglobulins

Antibodies bound to a cell surface antigen can induce cell death bound to the antibody by three different mechanisms.

  • First, an antibody bound to a cell surface can activate the complement system and create pores in the membrane of a foreign cell.
  • Second, antibodies can mediate cell death via antibody-dependent cell-mediated cytotoxicity (ADCC). In this process, cytotoxic cells with Fc receptors bind to the Fc region of antibodies on target cells and promote cell death.
  • Finally, thatantibodyalso attached to a foreign cellmeetB. as an opsonin, whereby phagocytic cells with Fc or C3b receptors can bind and phagocytose the antibody-coated cells


  • Blood transfusion/transfusion reactions: When transfused with incompatible blood, a transfusion reaction occurs due to the destruction of the donor's red blood cells by isohemagglutinins against the foreign antigen.
  • Eritroblastose fetal:It develops when maternal antibodies specific to fetal blood group antigens cross the placenta and destroy fetal red blood cells. As a result, severe hemolysis occurs, leading to anemia and hyperbilirubinemia, which can even be fatal.
  • drug-induced hemolysis: Certain drugs (such as penicillin, quinidine, phenacetin, etc.) can induce hemolysis of red blood cells. They adhere to the surface of red blood cells and induce the formation of IgG antibodies. These autoantibodies then react with the surface of the red blood cells, causing hemolysis.


Redness and swelling are the main symptoms of this category. It usually occurs somewhere between minutes and hours.


Treatment includes anti-inflammatory and immunosuppressive agents.


Type III reactions are the result of antigen-antibody immune complexes inducing an inflammatory response in tissues. The reaction between the different antigens and antibodies in the body leads to the formation of immune complexes. Under normal conditions, the mononuclear phagocyte system eliminates these immune complexes through the involvement of red blood cells.

In certain cases, these immune complexes are outside the range of phagocytic clearance. This allows them to grow and cause disease.

Deposition of immune complexes occurs in:

  1. in the walls of the blood vessels
  2. in the synovial membrane of the joints
  3. in the glomerular basement membrane two lavages
  4. in the choroid plexus of the brain
  5. sometimes immune complexes form at the site of inflammation

Immune complexes fix and activate the complement system. Complement fixation leads to the production of the chemokines C3a and C5a of the anaphylatoxins, which stimulate anaphylatoxinsthrowof vasoactive amines. C5a attracts neutrophils to the site, but these neutrophils cannot engulf a large total mass of immunity.Complex,and instead release lysosomal enzymes and lytic substances that damage host tissues.


  • Arthur's reaction
  • Serum sickness


As a result of type III hypersensitivity, the accumulation of complexes in the tissues can lead to symptoms such as fever, skin rash, joint pain, enlarged lymph nodes and protein in the urine.


It usually takes 3 to 10 hours for symptoms to appear.


Treatment includes anti-inflammatory agents. In addition, immunosuppressive drugs such as methotrexate and cyclosporine are also used in some cases.


it can also be called delayed-type cell-mediated hypersensitivity reactions. Begins hours or days after primary antigen exposure and usually lasts several days. In this response there is a large influx of non-specific inflammatory cells, mainly macrophages. It differs from other types of hypersensitivity in that it is mediated by cell-mediated immunity. This response occurs due to activation of specifically sensitized T lymphocytes rather than antibodies.

In 1890, Robert Koch observed this type of hypersensitivity in tuberculosis as a local reaction. It is also known as the tuberculin reaction. It was later recognized that the response could be induced under various pathological conditions and was renamed tolatetype of hypersensitivity.

The DTH (delayed-type hypersensitivity) response begins with an initial priming by the antigen, followed by a period of at least 1 to 2 weeks. During this phase, antigen-specific T cells are activated and clonally expanded. TH1 subtypes of CD4 cells are activated during the sensitization phase.

There are two types of DTH reactions:

  1. contact hypersensitivity
  2. Tuberculin-type hypersensitivity reactions

1. Contact hypersensitivity

Contact hypersensitivity is a type IV hypersensitivity. Occurs after sensitization with certain substances. For example, certain drugs such as sulfonamides and neomycin, an ingredient in a cosmetic or hair dye, a metal ion such as nickel, soaps, and other substances.

This reaction occurs when these substances penetrate the skin and combine with the body's own proteins to form complete antigens to which the person becomes sensitized. On the second exposure to the same antigen, the immune system responds by attacking cytotoxic T cells, which cause damage primarily in the skin.

The condition manifests as itching, erythema, blisters, eczema, or skin necrosis within 12 to 48 hours after the second exposure. Currently, the best way to avoid a DTH reaction is to avoid the causative antigen. After hypersensitivity develops, topical or oral corticosteroids are used to suppress the destructive immune response.

2. Tuberculin-type hypersensitivity reaction

The tuberculin reaction is a typical example of delayed hypersensitivity.

Tuberkulin-Hauttestdetermines whether or not a person has previously been exposed to Mycobacterium tuberculosis. In this test, a small amount of tuberculin protein is injected intradermally. If the skin at the injection site develops a red, firm, slightly swollen lesion after 48 to 72 hours, this indicates a positive test.

There are several other skin tests to detect DTH. This includes many skin tests for bacterial, fungal, viral, and helminthic infections.


Symptoms include redness and stiffness along with pain.


In vivo diagnostic tests include delayed skin resistance. For example the Montoux test and the patch test. In addition, delayed hypersensitivity testing or biopsy involves mitogenic reactions.

TYPE VOVERSENSITIVITY (stimulating type)

Antibodies bind to antigens on the cell surface, induce cells to proliferate and differentiate, and increase the activity of effector cells. The type V hypersensitivity reaction plays an important role in the pathogenesis of Graves' disease, in which excessive amounts of thyroid hormones are produced. In addition, the long-acting thyroid-stimulating antibody binds to thyroid-stimulating hormone (TSH) receptors on the surface of a thyroid cell. Interaction with the TSH receptor produces an effect similar to that of TSH, leading to excessive production and secretion of the thyroid hormone responsible for itgravesIllness.


Textbook of Microbiology and Immunology by Subhash Chanda Parija, page #149-155.

Also, in Kuby's Immunology, 7th edition, chapter no. fifteen



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