Type I hypersensitivity reactions, also known as immediate hypersensitivity reactions, are the most common type. They are mediated by IgE antibodies and mast cells, and can cause symptoms such as sneezing, runny nose, itchy eyes, and difficulty breathing.

Type II hypersensitivity reactions, also known as cytotoxic hypersensitivity reactions, are caused by the binding of antibodies to cell surface antigens, leading to complement activation and cell lysis. This can occur in blood transfusions, when the recipient's antibodies attack the donor's red blood cells.

Type III hypersensitivity reactions, also known as immune complex hypersensitivity reactions, are characterized by the formation of immune complexes that deposit in tissues, leading to inflammation and tissue damage. This can occur in diseases such as lupus and rheumatoid arthritis.

Type IV hypersensitivity reactions, also known as cell-mediated hypersensitivity reactions, are mediated by T cells and involve a delayed response, typically taking several days to develop. This type of reaction is involved in contact dermatitis and tuberculin skin tests.

Mast cells play a crucial role in Type I hypersensitivity reactions by releasing histamine and other inflammatory mediators, such as leukotrienes and prostaglandins, upon activation by allergens.

IgG is the primary immunoglobulin involved in Type II hypersensitivity reactions, where antibodies bind to cell surface antigens and activate complement, leading to cell lysis.

In Type III hypersensitivity reactions, the complement system plays a role in forming immune complexes with antigens, which can then deposit in tissues and cause inflammation.

Th1 cells are the primary T cell subset involved in Type IV hypersensitivity reactions, where they release cytokines that activate macrophages and other immune cells to mediate delayed-type hypersensitivity responses.

Cytokines play a crucial role in hypersensitivity reactions by promoting inflammation, recruiting immune cells to the site of reaction, and activating various effector mechanisms.

Type I hypersensitivity reactions, specifically IgE-mediated reactions, are commonly associated with penicillin allergy. Upon exposure to penicillin, IgE antibodies bind to mast cells, leading to degranulation and release of inflammatory mediators, causing symptoms such as hives, swelling, and difficulty breathing.

Antihistamines work by inhibiting the release of histamine from mast cells, thereby reducing the inflammatory response associated with Type I hypersensitivity reactions.

Type IV hypersensitivity reactions, particularly delayed-type hypersensitivity reactions, are characterized by the formation of granulomas, which are collections of immune cells that surround and attempt to contain foreign substances or pathogens.

T regulatory cells (Tregs) play a crucial role in regulating immune responses and preventing excessive inflammation. In hypersensitivity reactions, Tregs can suppress immune responses and help maintain immune tolerance.

Type IV hypersensitivity reactions, specifically allergic contact dermatitis, are associated with contact dermatitis. This occurs when an individual comes into contact with an allergen, leading to a delayed-type hypersensitivity response characterized by skin inflammation and redness.

Desensitization in Type I hypersensitivity reactions primarily involves the administration of blocking antibodies, which bind to allergens and prevent their interaction with IgE antibodies on mast cells, thereby reducing the release of inflammatory mediators.