Team 1's informative mind map by Hanna Qistina

Type 1 hypersensitivity: Immediate (hanna)

hannaqistinaf — 2024-07-31 02:08:59 UTC

Initiator of reaction (chokka)

hannaqistinaf — 2024-07-31 02:10:11 UTC

The reaction is initiated by the binding of autoantibodies IgG (sometimes IgM) to soluble antigens to form immune complexes, which are deposited in various tissues.

Neutrophils are then recruited, and inflammation is present at the sites where the immune complexes are deposited, causing tissue destruction and inflammatory reactions

Components of immune system involved (chokka)

hannaqistinaf — 2024-07-31 02:11:01 UTC

The components of the immune system that are involved are

Antibodies, which form immune complexes with the allergens, also known as antigens
Neutrophils, which are recruited to the site where the immune complexes are deposited, kickstarting the classical signalling pathway and inflammatory reaction through the secretion of cytokines such as CCL2 and IL-1b

Symptoms (Chokka)

hannaqistinaf — 2024-07-31 02:11:11 UTC

Some symptoms of type III hypersensitivity include:

Purpuras, which are small, non-blanching hemorrhages on the skin
Rheumatoid nodules
A flushed rash on the face
Joint pain and swelling
Rashes
Fever
Kidney damage
Urticaria (also known as hives

Possible treatment (Chokka)

hannaqistinaf — 2024-07-31 02:11:22 UTC

Treatment for type III hypersensitivity largely involves immunosuppression which includes:

Adrenaline, or epinephrine
Systemic glucocorticoids
Antihistamines
Disease-modifying antirheumatic drugs, such as methotrexate, cyclosporine, and cyclophosphamide
Biologic agents, such as TNF-blockers

THE TYPES OF HYPERSENSITIVITY REACTION

hannaqistinaf — 2024-07-31 02:11:56 UTC

Type IV hypersensitivity: Delayed type (danielle)

hannaqistinaf — 2024-07-31 02:12:53 UTC

Type IV hypersensitivity or delayed-type hypersensitivity(DTH) involves a T-cell-mediated immune response rather than antibody-mediated. It takes around 24-72 hours to developed exposure to the antigen and the reaction could take up to 3 to 4 weeks

Initiator of reaction (hanna)

hannaqistinaf — 2024-07-31 02:13:24 UTC

Allergen Exposure: The reaction is initiated by exposure to an allergen, which is a typically harmless substance that triggers an immune response in susceptible individuals. Common allergens include pollen, dust mites, animal dander, insect stings, certain foods (e.g., peanuts, shellfish), and drugs (e.g., penicillin).

Components of immune system involved (hanna)

hannaqistinaf — 2024-07-31 02:13:36 UTC

IgE Antibodies: The immune response begins with the production of IgE antibodies specific to the allergen. Upon first exposure, these IgE antibodies are produced and bind to the surface of mast cells and basophils.
Mast Cells and Basophils: These cells have high-affinity receptors for IgE (FcεRI). Upon subsequent exposure to the same allergen, the allergen binds to the IgE on these cells, causing them to degranulate.
Release of Mediators: Degranulation releases various pre-formed mediators like histamine, tryptase, and newly synthesized mediators such as leukotrienes, prostaglandins, and cytokines (e.g., IL-4, IL-5, IL-13).

Symptoms (hanna)

hannaqistinaf — 2024-07-31 02:13:48 UTC

Immediate Phase (minutes after exposure): Symptoms result from the release of histamine and other mediators from mast cells and basophils.
- Respiratory Tract: Sneezing, nasal congestion, runny nose (rhinitis), itchy eyes, throat irritation (common in hay fever).
- Skin: Urticaria (hives), itching, redness, and swelling.
- Gastrointestinal Tract: Nausea, vomiting, abdominal pain, diarrhea (common in food allergies).
- Systemic: Anaphylaxis, which can include widespread vasodilation, drop in blood pressure (shock), bronchoconstriction (difficulty breathing), and potentially fatal outcomes if not treated promptly.
Late Phase (hours after exposure): Involves recruitment of eosinophils, neutrophils, and other inflammatory cells leading to sustained inflammation and tissue damage. Symptoms may include chronic asthma or atopic dermatitis.

Possible treatment (hanna)

hannaqistinaf — 2024-07-31 02:13:57 UTC

Acute Management:
- Epinephrine (Adrenaline): First-line treatment for anaphylaxis. It works by vasoconstriction, bronchodilation, and increasing cardiac output.
- Antihistamines: Such as diphenhydramine or cetirizine, which block histamine receptors and reduce symptoms like itching and hives.
- Corticosteroids: Systemic corticosteroids (e.g., prednisone) can reduce inflammation and are used in more severe cases.
- Bronchodilators: Such as albuterol for asthma symptoms, to relax bronchial smooth muscles and improve breathing.
Long-term Management:
- Avoidance of Known Allergens: Identifying and avoiding triggers can prevent reactions.
- Allergen Immunotherapy (Desensitization): Gradual exposure to increasing amounts of the allergen to build tolerance.
- Monoclonal Antibodies: Omalizumab (anti-IgE) can be used in severe asthma or chronic urticaria to reduce IgE levels and prevent mast cell degranulation.
- Education and Emergency Plan: Educating patients and caregivers on recognizing symptoms and using emergency medications like auto-injectable epinephrine (e.g., EpiPen).

Type II hypersensitivity: Cytotoxic (aikin)

hannaqistinaf — 2024-07-31 02:14:11 UTC

Initiator of reaction (danielle)

hannaqistinaf — 2024-07-31 02:14:52 UTC

Antigens in DTH are small molecules referred to as hapten where they penetrate the skin and bind to proteins. This causes it to form complexes that are recognized as foreign:

Antigens that are environmental:

Urushiol in poison Ivy--> Urushiol binds to proteins in the skin and alters the protein, making the immune system recognize these changed proteins as foreign, this causes a reduced number of proteins to be needed for immune complexes, other plant resins including poison oak and poison sumac which similarly initiates this reaction

Autoantigens:

self-antigens that are mistakenly targeted by the immune system leading to autoimmune diseases. In DTH T cells recognize these autoantigens as foreign resulting in chronic inflammation and tissue damage. --> e.g, would be beta cell antigens, which are targeted by T cells in the pancreas, causing a deficiency in insulin

Initiator of reaction (aikin)

hannaqistinaf — 2024-07-31 02:14:57 UTC

Antibodies: Type II hypersensitivity is mediated by antibodies, such as IgG and IgM, directed against antigens on host cells, which causes cell and tissue destruction by complement activation (classical pathway) or antibody dependent cell-mediated cytotoxicity. For example, Antibody-Dependent Cell Cytotoxicity (ADCC) via IgG with NK cells, or phagocytes. Type II hypersensitivity is a type of immune response in which the immune system attacks the body's own cells or tissues.

Components of immune system involved (danielle)

hannaqistinaf — 2024-07-31 02:15:03 UTC

1. T cells :

--> CD4+ T helper cells such as Th1 and Th17

--> they can recognize the antigen presented by APCs which are antigen-presenting cells and secrete cytokines such as interferon-gamma(IFN-γ) & IL-17.

--> The sensitized Th1 cells release cytokines that activate the macrophages (phagocytes) leading to an inflammatory response where they undergo phagocytosis

--> Th1 cells take several days to become fully active where the Th1 effector cell recognizes the processed antigens and releases cytokines that act on the vascular endothelium

2. CD8+ cytotoxic T cells (Tc cells)

--> These cells kill infected cells, presenting the antigen via MHC class I molecules directly and thus mediating direct cellular damage.

3. APCs - anitgen-presenting cells

--> dendritic cells capture the antigens and present them to T cells to initiate the immune response and migrate to lymph nodes to interact with the T cells or naive T cells which will then present a portion of the protein using MHC class 2 receptors to allow naive T helper cells to recognize and bind to after binding of APC to the naive T helper cell

--> certain cytokines are released from the naive T helper cell to differentiate into a type 1 T helper cell releasing interferon-gamma(IFN-γ) which is a cytokine, a mediator.

Components of immune system involved (aikin)

hannaqistinaf — 2024-07-31 02:15:10 UTC

Antibodies IgG and IgM: IgG and IgM are the main mediators of type 2 hypersensitivity. They are produced by B cells and specifically bind to antigens present on the surface of cells or extracellular matrix.
Antigens: In type 2 hypersensitivity, the antigens that antibodies target are typically specific molecules or markers found on the cell surface or within the extracellular matrix. This can include Rh antigen, acetylcholine receptors, drug molecules and autoantigens.

Phagocytes: Cells such as macrophages and neutrophils can identify and engulf antibody-coated cells or cellular debris through the process of phagocytosis.
Natural Killer (NK) Cells: NK cells release perforin and granzymes to kill a target cell. Perforin creates an opening in the target cell so the NK cell can insert granzymes. The granzyme kills the cell.

Symptoms (danielle)

hannaqistinaf — 2024-07-31 02:15:16 UTC

Contact Dermatitis
- Redness and itchy rash
- Swelling
- Blisters and Hives
Inflammation of Granulomatous
- cluster of macrophages that form granulomas causing infections that are chronic such as tuberculosis --> causing erythema due to tissue damage and inflammation, and sarcoidosis --> when leukocytes like T cells and macrophages, etc., infiltrate a site of antigen exposure and cause a delayed form of inflammatory tissue damage
- Further leading to persistent cough, weight loss, and even fever
Autoimmune reactions
- such as organ dysfunction --> including joint pain and swelling in rheumatoid arthritis and multiple sclerosis which causes neurological symptoms

Symptoms (aikin)

hannaqistinaf — 2024-07-31 02:15:48 UTC

Autoimmune Hemolytic Anemia:
- Fatigue
- Pallor
- Shortness of breath
- Jaundice
Immune Thrombocytopenic Purpura (ITP):
- Easy bruising
- Petechiae (small red or purple spots on the skin)
- Excessive bleeding from minor cuts
- Frequent nosebleeds or gum bleeding
Anaphylactic shock
Watery Eyes
Itching
Redness
Swelling
Nausea and Vomiting: Feeling queasy and the act of forcefully expelling stomach contents.
Diarrhea: Frequent, loose, or watery bowel movements.
Constipation: Difficulty passing stools or infrequent bowel movements.
Abdominal Pain: Discomfort or pain in the stomach or abdominal area, which can be sharp, crampy, or dull.
Indigestion (Dyspepsia): Discomfort or pain in the upper abdomen, often associated with bloating, fullness, and nausea.

Possible treatment (danielle)

hannaqistinaf — 2024-07-31 02:16:03 UTC

Topical corticosteroids --> to reduce inflammation and alleviate symptoms for contact dermatitis

Systemic corticosteroids --> more severe reactions and is taken orally to reduce internal inflammation of body

Immunosuppressive drugs--> example TNF inhibitors which can be used in diseases such as rheumatoid arthritis and psoriasis

Antibiotics or Antimicrobial drugs --> for example antitubercular drugs to reduce the spread of tuberculosis and kill the causative agent Mycobacterium tuberculosis

Desensitization therapies --> to increase T cells (Tregs) to suppress the allergic responses. It is also to increase the allergen-specific IgG antibodies (such as IgG4 Ab) which can block allergens from binding to IgE on mast cells and basophils preventing allergic reaction

Type III hypersensitivity: Immune Complex (chokka)

hannaqistinaf — 2024-07-31 02:16:23 UTC

Type III hypersensitivity involves the formation of immune complexes composed of antigen-antibody complexes. The reaction time is approximately 3-10 hours after initial exposure.

The immune complexes formed can accumulate in different types of tissues and trigger an inflammatory response, causing damage to the tissue/s involved. Active complements and immune cells will be recruited as well, which leads to tissue inflammation and injury.

Possible treatment (aikin)

23000394_2 — 2024-07-31 03:39:39 UTC

Immunosuppressants (e.g. corticosteroids or azathioprine)
systemic glucocorticoids
cyclophosphamide and cyclosporin agents
intravenous immunoglobulin infusions
plasmapheresis (remove some plasma from the blood, exchanging for a healthier one)

Avoid taking these drugs (common causes of Type II Hypersensitivity)
- penicillin
- methyldopa
- thiazides
- cephalosporins

resources

daniellethomas005 — 2024-07-31 10:39:36 UTC

Republic poly immunology lesson 12 scorm package
https://ditki.com/course/pathology/glossary/term/hypersensitivity-type-iv
https://dermnetnz.org/topics/allergies-explained
https://youtu.be/kQFmrQfBW5k?si=EvnI6Dqa-p3l_XbX