Life SciencesImmunologyPathologyAutoimmunityHost-pathogen InteractionsImmunopathologyAutoimmune Disease PathogenesisAutoimmune DiseasesCytokine-mediated PathologyImmune-mediated DiseaseT Cell ActivationT Cell BiologyB Cell-mediated PathologyCytokine-induced Immune ActivationCytokine-mediated Immune ModulationCytokine-mediated Immune RegulationHuman Leukocyte Antigen-b51Immune Stress ResponseImmunopathological MechanismsMhc-linked Disease Associations
A working hypothesis is postulated for the immunopathogenesis of Behçet's disease (BD). Microbial infection induced stress upregulates HSP65 and MICA gene product which stimulate gamma delta and alpha beta T cell receptor positive cells, to generate effector and suppressor T cells (fig. 1). These activated T cells, antibodies and neutrophils induce cytokines to modulate the immune response. The end result of these complex cellular and cytokine immune interactions in HLA-B51 or genetically related subjects is to induce pathological changes consistent with BD.