#Type 3 hypersensitivity reaction skin#

Doctors use skin and blood tests to diagnose allergies. Anaphylaxis is a severe reaction that can be life-threatening. Allergies can range from minor to severe. Genes and the environment probably both play a role.Īllergies can cause a variety of symptoms such as a runny nose, sneezing, itching, rashes, swelling, or asthma. In most allergic reactions, however, it is responding to a false alarm. Normally, your immune system fights germs. Substances that often cause reactions are People who have allergies often are sensitive to more than one thing. Īn allergy is a reaction by your immune system to something that does not bother most other people. Vaillant (2021) Delayed Hypersensitivity Reaction, StatPearls, accessed įunctions of the body's response of increased sensitization to foreign substances, such as in sensitivities to different antigens.Īn inflammatory response to an exogenous environmental antigen or an endogenous antigen initiated by the adaptive immune system.Immune Allergic Contact Dermatitis after prior Mycobacterium tuberculosis exposure.Autoimmune cell-mediated destruction of Insulin-secreting pancreatic beta cells.Cytokines trigger Phagocytosis and inflammation.Interferon-gamma) and CD8+ cells may destroy Antigen directly Activated T Lymphocytes release Cytokines (e.g.Antigen bound to Major Histocompatibility Complex (MHC) on Antigen Presenting Cells.Triggering initial Antigens are often infectious ( Mycobacteria, protozoa, and fungi).Mediated by Effector T Lymphocytes (CD4+ and CD8+), activated in response to specific Antigens.

Reaction within 2-7 days after exposure.

Typically due to Viral Hepatitis Antigen (esp.

Elephantiasis (Wuchereria bancrofti reaction).

Serum Sickness (prototypical Immune Complex Reaction).

Joint synovial membranes resulting in Arthritis.

Renal glomerular basement membrane resulting in nephritis.

Blood vessel walls resulting in Vasculitis.

Small immune complex deposition results in inflammatory reaction within 1-3 weeks of exposure.

Lysosomal enzyme secretion damages normal tissue.

Other injury mechanisms triggered by immune complexes.

These complexes may instead precipitate, deposit in tissue with inflammation.

However, small complexes may be missed by Phagocytosis.

These complexes are then typically destroyed by phagocytic cells (PMNs, Macrophages).

Most immune complexes typically activate the complement system.

Contrast to typical immune complex processing.

Antigen- Antibody immune complexes deposit in tissue.

Autoantibodies to renal glomeruli and pulmonary alveoli.

Autoantibodies to acetylcholine receptors on Neurons.

Autoantibodies to gastric intrinsic factor (required for Vitamin B12 absorption).

Autoantibodies to Platelet surface proteins.

Autoantibodies to Red Blood Cell membrane proteins.

Mycoplasma pneumoniae related cold Agglutinins.

Rhesus Incompatibility (Rh Incompatibility).

Transfusion Reaction ( ABO Incompatibility).

Antibody- Antigen complexes by lysis or phagocytocsis.

IgG binds Antigen and activates complement.

Antibodies bind infected cells with surface Antigen, targeted for Natural Killer Cell-mediated destruction.

Antibody-dependent cellular cytotoxicity (ADCC).

Antibody-bound Antigen ( Opsonin) is destroyed by cells (PMNs, Macrophages) engulfing complex ( Phagocytosis).

Antibody- Antigen Complex destruction by one of three mechanisms.

Mediated by IgG and IgM (on cell surface or extracellular complex) to specific Antigens.

Inflammatory cell infiltration ( Eosinophils, Neutrophils, T-Cells).

Late Phase (2 to 24 hours after exposure).

Histamine-induced vasodilation, edema, congestion.

Early Phase (within minutes of exposure, <1 hour).

Although there are four histamine receptors (H1, H2, H3, H4), H1 predominates in Type I Reaction.

Release secretory granules including histamine (as well as leukotrienes, prostaglandins).

Mast Cells and Basophils are then stimulated with repeat exposure.

Mast Cells are now sensitized, awaiting allergan reexposure.

IgE binds blood Basophils and tissue Mast Cells at the high affinity Fc receptor (FceRI).

B-Cells produce the IgE against the specific Antigen.

B-Cells class switch to produce IgE Antibody against Antigen (instead of IgG and IgM).

B-Cells are are exposed to Antigen (e.g.

Mediated by IgE Antibody to specific Antigens.

Most common form of Hypersensitivity Reaction.

Immediate allergan immune response after repeated exposure (esp.

Type 3 hypersensitivity reaction