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Types of Hypersensitivities - Coggle Diagram
Types of Hypersensitivities
Type 1: Immediate Hypersensitivity
mechanism of tissue injury & disease:
mediated by previously
sensitized B lymphocytes
: mast cells & their mediators (vasoactive amines, lipid mediators, cytokines), eosinophils
important molecules:
IgE antibody, Th2, Th2-like, Tfh
immediate reaction mediators: histamine, prostaglandins, leukotrienes
Clinical examples/ symptoms
systemic anaphylaxis
acute urticaria
sudden-onset skin reaction characterized by itchy, raised, red or skin-colored welts (also called hives)
Allergic rhinits (hay fever)
Edema of nasal mucosa irritation of nasal mucosa
Asthma (attack)
Food Allergy
vomiting, diarrhea, pruritis (itching), urticaria (hives), anaphylaxis is possible but rare
Type 2: Antibody Mediated
Mechanisms of tissue injury & disease
Opsonization & phagocytosis of cells --> Lysis via
membrane-attack complex formation
Complement & Fc receptor mediated recruitment & activation of leukocytes (neutrophils, macrophages)
Important molecules
IgM, IgG antibodies against cell surface or extracellular matrix antigens; abnormalities in cellular functions
Clinical Examples
Anemia
Penicillin-induced hemolytic anemia
Autoimmune hemolytic anemia
autoimmune thrombocytopenia purpura
pernicious anemia
ABO blood mismatch
Skin vesicles
eg. emphigus vulgaris
Different inflammation diseases
Vasculitits
nephritis, lung, hemorrhage
Good pastures disease
Myasthenia gravis
Disease Mechanism: Antibody inhibits acetylcholine binding down-modulating receptors & causing
muscle weakness/ paralysis
Graves disease
Hyperthyroidism antibody binding to TSH receptor
SLE
mnemonic:
antibody against me and you!
Type 3: Immune Complex Mediated
mechanism of tissue injury & disease:
mnemonic:
antigen-antibody complex is free
Deposition in blood vessel walls/ tissue!
Complement & Fc receptor- mediated recruitment & activation of
leukocytes in blood vessel walls/ tissues
Important molecules IgM or IgG
Clinical Examples
Drug induced auto-immunity
Some antibiotics/anti-mcirobials (e.g., penicillin, etc)
Drugs from foreign source (e.g., made in different species)
Some drugs
Drug Induced SLE
rxns to foreign antigens (could also be environmental)
Serum Sickness:
After “passive” immunization with anti-serum/antibodies produced from a foreign source in polyclonal and monoclonal (e.g., non-human source, other human)
Some viral infections (e.g., hepatitis B, etc)
Tumor antigens
causing damage to skin, kidney, joint, & serousal damaged
SLE
Type 4: T-cell mediated
Important molecules
CD4+ T cells; Th1 & Th17; CD8+ CTLs (T cell--mediated cytolysis)
macrophages
Clinical Examples
contact mediated reactions
induced by haptens such as
nickel, poison ivy
(pentadecacatechol) & any small molecule that can penetrate skin & conjugate with carrier proteins
Eczematous reactions --> contact with allergens
Multiple Sclerosis
Protein antigens in myelin (e.g., myelin basic protein); causes Demyelination in CNS with perivascular inflammation; paralysis, ocular lesions
Rheumatoid arthritis
collagen t-cells lead to destruction of articular cartilage and bone
Type 1 diabetes mellitus
Hashimoto thyroiditis: Hypothyroidism
Inflammatory bowel disease
Autoimmune myocarditis: Cardiomyopathy
Sjogren's Syndrome
T-cell mediated destruction of lacrimal and salivary glands
causing
dry eyes, dry mouth
, also systemic manifestations
Clinical findings
Lip biopsy
Auto antibodies to Ribonucleoproteins SS- A (Ro) & SS-B(La) up to 90%
Positive for rheumatoid factor (anti-IgG auto-antibody)
detected ANAs (anti-nuclear antibodies)
Graft vs. Host Disease
Mechanism of tissue injury & disease
1) Macrophage activation, cytokine-mediated inflammation
2) Direct target cell killing, cytokine-mediated inflammation
Hyperacute Rejection: w/in min - hours of blood transplantation