Allergens are substances that trigger allergic reactions in individuals with a hypersensitive immune response. One allergen class, airborne allergens, includes, pollen, mould spores, dust mites and animal dander. Common food allergens include peanuts, tree nuts, milk, eggs, wheat, and soy. Venom from bee and wasp stings can similarly trigger allergic reactions, ranging from mild to severe (anaphylaxis), whilst medication allergens include antibiotics (e.g., penicillin), non-steroidal anti-inflammatory drugs (NSAIDs), and certain vaccines. Moreover, occupational allergens encountered in the workplace, such as latex, chemicals, and dust, can also lead to allergies in susceptible individuals. By sharing structural features some allergens also exhibit cross-reactivity, with individuals allergic to pollen for example, experiencing cross-reactivity to certain fruits and vegetables. Determining how allergens interact with the immune system is important in understanding immunological mechanisms underlying allergic reactions, diagnosing allergies, and developing treatments. Allergen exposure to the immune system begins with initial allergen sensitization, whereby the allergen triggers the immune system to recognize it as foreign. Antigen-presenting dendritic cells first capture and process protein allergens, presenting their peptide fragments on their cell surfaces using major MHC molecules. T helper cells (Th cells), particularly Th2 cells, then recognize these allergen-MHC complexes and become activated. Activated Th2 cells subsequently release cytokines, including interleukin-4 (IL-4), interleukin-5 (IL-5), and interleukin-13 (IL-13) which in turn stimulate B cells to produce allergen-specific immunoglobulin E (IgE) antibodies. IgE antibodies produced by B cells can then bind to high-affinity IgE receptors (FcεRI) expressed on the surface of two specialized immune cells; mast cells, located in tissues that are in contact with the external environment or potential allergens, such as the skin, respiratory tract, digestive tract, and mucous membranes; and basophils, circulating in the blood. During subsequent exposure to the same allergen, the allergen binds to IgE antibodies already bound to mast cells or basophils. When multiple IgE antibodies on these cells recognize an allergen, they cross-link, triggering the release (degranulation) of granules containing histamine, leukotrienes, prostaglandins, and other inflammatory mediators. Degranulation is itself triggered by signalling pathways downstream of FcεRI crosslinking that lead to an increase in intracellular calcium levels, promoting the fusion of granules with the cell membrane. The release of inflammatory mediators leads to rapid effects, such as vasodilation (increased blood vessel diameter), increased vascular permeability, smooth muscle contraction (bronchoconstriction), and itching, resulting in the classic symptoms of allergy. Following the immediate response, a late-phase reaction may also occur, characterized by the cytokine-induced recruitment of other immune cells like eosinophils, neutrophils, and T cells. The activation of eosinophils and other cells contributes to the tissue damage and chronic inflammation seen in some allergic conditions such as asthma. Some allergens share protein features, leading to cross-reactivity, and explaining why individuals allergic to certain pollens can also react to certain fruits. In some cases, allergic reactions may be controlled by desensitization (immunotherapy) involving controlled exposure to gradually increasing amounts of allergens. This approach aims to induce immune tolerance by promoting the production of blocking IgG antibodies and altering Th2 responses, reducing allergic symptoms. We provide a comprehensive product catalogue of research reagents for investigating allergens, including HLA G antibodies, TIM 1 antibodies, HRH1 antibodies, TCTP antibodies, and TIM 1 ELISA Kits. Explore our full allergens product range below and discover more, for less.