Kumar Lav Kush Tarun
Magadh University, India
Posters-Accepted Abstracts: J Clin Cell Immunol
A widespread category of people whose quality of life is affected by a medical condition is the one representing patients with disorders related to thyroid gland function. Described as having multiple causes (from iodine deficiency to postpartum status), thyroid disease affects a significant number of people and it can be seen in any age group. The challenges in front of a patient with thyroid dysfunction (TD) are recording (qualitative or quantitative) alterations of hormonal secretion of the thyroid gland structure, differentiation of psychological effects caused by the manifestation of the disease from the ones caused by specific medication and the importance the patient gives to life events. It is well known that the principle effectors of the immune system are B and T lymphocytes and those lymphocytes can be divided into T-helper (Th) cells, which express CD4+ surface antigens, and T-cytotoxic (Tc) cells, which express CD8+ surface antigens. The CD4+ Th precursor cells are further subdivided into two populations, Th1 and Th2 cells. Th1 cells secrete interleukin-2 (IL-2), interferon-Ï? (IFN-Ï?) and tumor necrosis factor alpha (TNF-?±), which regulate the cellular-mediated immune response and the induction of tissue damage. Th2 cells secrete interleukins, IL-4, IL-5, IL-6 and IL-10 and are activated to provide help to B lymphocytes for specific immunoglobulin (Ig) production. Thyroid autoimmunity has been shown to occur via a two stage process. Stage one involves the increased appearance of intra-thyroid antigen presenting cells (APC) that carry and present thyroid auto-antigens to Th cells. Stage two involves lymphocytes interacting with the presented autoantigens, leading to the generation of a large number of autoreactive CD4+ Th lymphocytes, CD8+ Tc lymphocytes and antibody-producing B lymphocytes that infiltrate the thyroid parenchyma. This turns the thyroid gland into a 'battlefield' where the outcome of the interaction between the thyrocytes and infiltrating lymphocytes determines the different clinical outcomes of AITD, believed to be due to differences in the cytokines profile in the thyroid gland upon infiltration . In AIH there appears to be a prevalence of Th1 cytokines, leading to a predominance of T lymphocyte immunity, causing increased immune destruction of the thyroid cells and hypothyroidism. In GD, on the other hand, there appears to be a predominance of Th2 type inflammatory cytokines and B lymphocyte immunity producing high levels of IgG antibodies specific for the TSHR which can activate the receptor, causing thyroid cell hyperplasia and hyperthyroidism. The fact however, that both diseases can develop in the same individual at different time points suggest that immunological categorizations may be overly simplistic and that cytokine patterns are dynamic processes. This review will focus on the genetic contribution to AITD which to a large extent involves the role of immune response genes.
Email: lktarun@gmail.com
