The platelet has traditionally been associated with haemostasis. Participation of platelets in defence mechanisms is presentiment by the knowledge that primary haemostasis may be phylogenetic vestige retained from the behaviour of primitive leukocytes. Platelets have the ability to undergo shape change with pseudopod formation, chemotaxis, diapedesis, and phagocytose. Platelets contain a wide range highly potent inflammatory factors that are capable of inducing or augmenting certain inflammatory responses. Different surface molecules have been detected on the plasma membrane, highlight the platelets ability to bind a variety of biologic surfaces, including those of other cells, resulting in close apposition of platelets and their targets. They can interact with parasites, viruses and bacteria. Studies from several groups suggest an important role of the platelet in allergic processes. Platelets possess receptor for immunoglobulin E. Numerous clinical reports are describing the modification of biologic activity of platelets from allergic patients as compared to healthy subjects. The incidence of abnormal platelet responsiveness is in higher among patients having high serum IgE titres. Platelet depletion decreased the anaphylactic response and protects against the lethal consequences of the antigen provocation. Evidence now exists in support of primary role of the platelet in the pathogenesis of bronchial asthma. Platelets can participate in allergic asthma by acting as inflammatory cells, by releasing spasmogens and by interacting with other inflammatory cells. Thrombocytopenia and the increased plasma levels of platelet-derived markers occurred in parallel with bronchoconstriction induced by antigen provocation of allergic astmatics. Platelet depletion inhibits the ability of antigen to induce late onset airways obstruction and airway hyperresponsiveness. Platelet apheresis in human resulted in a positive clinical effect. Platelets respond to aspirin or other NSAIDs in acetyl salicylic acid sensitive asthmatics and these findings provide further evidence for role of the platelet in this form of bronchial asthma.