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(i) Initiator of reaction

Initiated by antigen-antibody complexes in bloodstream

These accumulate in tissues > activates complement and recruit immune cells (inflammatory response)

Leads to tissue damage

(ii) Components of immune system involved

Antibodies IgG, IgM

Neutrophils

Complement system

EXAMPLE OF DISEASE: Systemic lupus erythematosus (SLE)

type III hypersensitivity & autoimmune disease

(iii) Symptoms

fever

fatigue

joint pains

butterfly rash

hair loss

mouth ulcers

shortness of breath

swelling in legs/around eyes

kidney problems

neurological symptoms - headaches, seizure, stroke

(iv) Possible treatments

immunosuppressive drugs

corticosteroids - anti-inflammatory drug

antimalarial drugs - helps with joint pain, fatigue, rashes

Non-steroidal anti-inflammatory drugs (NSAIDs) - control fever, joint pains, swelling

Resources:

Systemic Lupus Erythematosus – Signs, Treatments | SingHealth

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Type I: Intermediate hypersensitivity - immediate (Dav)

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Type I: Intermediate hypersensitivity - immediate (Dav)

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(i) Initiator of reaction

Allergen with pre-exposure:

In the first exposure (initial) to the allergen, the allergens are phagocytosed by B cells which act as antigen-presenting cells (APCs) to present allergen peptides to naive T cells to activate them. These activated helper T cells then help to trigger the activated B cells to undergo class switching to produce IgE antibodies specific to the allergen. the IgE antibodies then bind to the Fc receptors on mast cell surface to sensitize them. --> IgE-mediated hypersensitivity response.

IgE antibodies have a specific region called Fc region, mast cells are immune cells which have high-affinity receptors for the Fc region of IgE, known as FcεRI (Fc epsilon receptor I). These receptors are present on the mast cell surface bind to the Fc region of IgE antibodies.

Once IgE antibodies are bound to the FcεRI receptors on the mast cells, the mast cell is considered sensitised. sensitization means that the mast cells are now primed and ready to respond to subsequent exposures to the same allergen. Upon re-exposure to the same allergen, the allergen binds to the IgE antibodies already attached to the FcεRI receptors on the mast cells. this binding causes cross-linking of the IgE molecules triggering the activation of mast cells to degranulate. Rapid degranulation releases various chemical mediators such as histamines, leukotriene and other inflammatory mediators.

(ii) Components of immune system involved

IgE antibodies - specific IgE produced in response to the allergen, central to the initiation of the hypersensitivity reaction

Mast cells - found in tissues throughout the body, have high affinity to the receptors of IgE, degranulate, release various inflammatory mediators

Basophils - white blood cell that has high-affinity receptors for IgE, can degranulate in response, circulate in the blood, function similar to mast cells

inflammatory mediators - e.g. histamine, causes vasodilation, vascular permeability, smooth muscle contraction, mucus secretion and oedema formation.

(iii) Symptoms

Gastrointestinal: vomiting, diarrhoea, nausea, stomach cramps

Respiratory: coughing, wheezing, phlegm, shortness of breath, swelling and mucus secretion in nasal passages

Systemic reaction: anaphylaxis, hypotension, shock

Skin: dermatological hives, oedema, soft tissue angioedema, itching

(iv) Possible treatments.

Antihistamine medication - blocks histamine's action from activated mast cell

Anti-inflammatory medication

Immunotherapy - desensitization therapy by injections of specific antigen, sublingual immunotherapy (SLIT) to place allergen tablets under the tongue as another method of desensitization

Corticosteroids - reduce inflammation, in the form of topical creams, oral medication or nasal spray

Bronchodilators - to alleviate respiratory symptoms

EpiPen (epinephrine auto-injectors) - epinephrine (adrenaline) for severe cases such as anaphylaxis

Resources:

https://www.sciencedirect.com/topics/immunology-and-microbiology/type-i-hypersensitivity

https://en.wikipedia.org/wiki/Type_I_hypersensitivity

https://pubmed.ncbi.nlm.nih.gov/32809396/

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Type Iv hypersensitivity reactions (Adrian and Jennifer)

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Type Iv hypersensitivity reactions (Adrian and Jennifer)

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Type II Hypersensitivity aka Cytotoxic (fitri)

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Type II Hypersensitivity aka Cytotoxic (fitri)

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(i) Initiator of reaction:

Rh antigen, acetylcholine receptors, drug molecules, autoantigens.

Depending on the type of antigen, it can significantly influence the mechanism of tissue damage — an example: Rh antigen.

Rh factor is a protein found on some red blood cells and not everyone carries this protein. Those who carry it are Rh-positive, while those who don't carry it are Rh-negative.

Rh incompatibility occurs when an individual (mother) is Rh-negative and another individual (father) is Rh-positive, conceive a baby who may have Rh-positive blood, inherited from the father.

Having a Rh-positive antigen on your red blood cell would enable your body to learn to recognise that antigen as being part of your body so that your body doesn't attack it. But when you're an Rh-negative, you don't have the Rh factor (protein) on your red blood cells, meaning that you don't have the protein on your red blood cells.

When Rh-positive blood (from fetus) and Rh-negative blood (from mother) comes into contact, the mother's immune system would recognize the Rh-positive antigen as foreign and her B cells would release anti-D antibodies which are a specific type of IgG antibody to attack the Rh-positive red blood cells in response.

These anti-D antibodies will then cross the placenta and bind to the fetus's Rh-positive red blood cells, initiating the destruction of their red blood cells through complement activation and antibody-dependent cell-mediated cytotoxicity (ADCC), resulting in a condition known as hemolytic disease of the newborn (HDN).

(ii) Components of immune system involved:

IgG or IgM antibodies (mainly IgG as they're small enough to cross the placenta).

(iii) Symptoms:

Pale skin.

Yellowing of the amniotic fluid, umbilical cord, skin, and eyes - due to jaundice, breakdown of red blood cells produces bilirubin (a brownish yellow substance) that is difficult for a baby to discharge and can build up in his blood (hyperbilirubinemia) and make his skin, eyes etc appear yellow.

Enlarged liver or spleen - baby's body tries to compensate for the breakdown of red blood cells by producing more of them quickly in the liver and spleen, resulting in enlargement.

Severe swelling of the body.

(iv). Treatments:

During pregnancy,

Blood transfusion - replaces fresh blood that has normal bilirubin level.

Early delivery of the baby if severe complications arise and baby's lungs are mature.

After birth,

Blood transfusion.

Intravenous fluids - restore and maintains fluid balance in the baby's body.

Oxygen or mechanical breathing machine .

Exchange transfusion to replace baby's damaged blood with fresh blood.

Resources:

Dean, L. (1970, January 1). Hemolytic disease of the newborn. Blood Groups and Red Cell Antigens [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK2266/#:~:text=The%20mother’s%20immune%20response%20to,delivered%20to%20the%20fetal%20circulation.

Hemolytic disease. Hemolytic Disease | Boston Children’s Hospital. (n.d.). https://www.childrenshospital.org/conditions/hemolytic-disease

Hemolytic disease of the newborn (HDN). Stanford Medicine Children’s Health. (n.d.). https://www.stanfordchildrens.org/en/topic/default?id=hemolytic-disease-of-the-newborn-hdn-90-P02368#:~:text=Exchange%20transfusion&text=It%20replaces%20it%20with%20fresh,getting%20small%20amounts%20of%20blood.

Reference to understand more about Rh incompatibility in pregnancy:

https://youtu.be/pwKqwcVNuMY?si=vYVN6WUGkucv1t1e