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Effect of concanavalin A (conA) on lymphocytes of thalasemmia patientLectins are proteins which were first detected in plant extracts; these proteins bind to carbohydrate moieties of complex macromolecules and binds reversibly to specific 2 E×ect of Concanavalin A (ConA) on lymphocytes of thalassemia Patients carbohydrate which is normally termed carbohydrate recognition domain (CRD) or carbohydrate binding domain (CBD). The property of lectin to bind carbohydrate at specific sites has distributed the lectins in all living organisms from virus to vertebrates. In the microbial world they are called by other names such as hemaglutinins, adhesion, and toxins. In animals, lectins present serve much different biological function such as cell adhesion, pathogen recognition, and glycoprotein synthesis. In leguminosae family of plant kingdom lectins are present abundantly. Lectins in plants found in tissues including seeds, roots, and fruits. And the lesser amount of lectins also also present in the bark, flower, and ovaries, and nectar but the seeds contains about upto 10-15% of the total protein content. Plants lectins can be easily extracted because of property of solubility. Concanavalin A is a plant lectin extracted from the jack beans (Canavalia ensiformis) has been extensively as a probe to study cell surface interaction and cell division. T cells respond to the concanavalin A (Con A ) only in the presence of Ia-positive accessory cells ( AC). There are two steps for the chain of events leading to T cell proliferation (a) Con A induces the production of interleukin 2 (IL2), a growth factor for activated T cells; it is now known that IL2 is produced by T cells of the helper (Lyt- 2-) phenotype; and (b) Con A induces reactivity to IL2 in resting T cells which then respond to IL2 with proliferation. β-Thalassemia is a blood genetic inherited disease from parents to offspring. B-thalassemia is can be broadly divided into three categories. [1] [2] (a) β-Thalassemia trait- the individual having one defective gene and one normal gene, individual don’t require transfusion but may have experience mild anemia. (b) β-Thalassemia intermedia– the individual having both defective gene but have some β- globin production and need intermittent transfusion. (c) β-Thalassemia major (Cooley’s anemia)- the individual have both gene defective and there is no β-globin production and the individual need lifelong transfusion of blood(RBC) and may have short lifespan[3] β-Thalassemia major patient need blood transfusion within the second birthday to prevent anaemia and physical consequences. The standard of transfusion should maintain hemoglobin level 10gm/dl. The combination of regular blood transfusion and chelation therapy improved overall survival of major patients. Thalassaemia patients have also option of bone marrow or stem cell transplantation but it is out of reach for most of the patients because of money problem hence they have only option of blood transfusion for treatment of thalassaemia. The thalassaemia patients have several complications due to multiple transfusion of blood the patient’s body start making or development of alloantibody against the donor RBC this is called alloimmunization. Alloimmunization further complicates in the problem of getting compatible blood, increased incidence of additional alloantibody and autoantibody (antibody against self RBC antigen). Alloimmunization rate of 5-30% has been found in thalassaemia patients and for prevention of the alloimmunization extended phenotype matched, lecodepleted red cell transfusion is recommended. The number of major thalassaemia patients in India is so high and data of alloimmunization is not through.