A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine. / The multifaceted phenotype of the B‐lymphocyte has a remarkably effective role in peptide derived pathogen clearance and the prevention of re‐infection. This mechanism of host tolerant defense can be attributed to the actions of particular cellular subsets that arise from Blymphocytes: memory cells and high‐affinity antibody secreting plasma cells. Notably B cell propagation does not commence without the help of follicular helper T cells (TFH), a specialized subset of CD4+ cells. TFH cells are involved in the maturation and differentiation of Blymphocytes after antigen stimulation with a thymus‐dependent peptide. With this specific stimulus the formation of germinal centers (GCs) within B‐cell follicles of secondary lymphoid organs is induced and it is within these centers that TFH cells are able to interact with B cells to facilitate immunoglobulin affinity maturation, somatic hypermutation, and isotype class switching. Importantly, these respective processes play a fundamental role in manufacturing high‐affinity antibodies for effective pathogen clearance. Conversely, by means not well understood, the occurrence of spontaneous GC formation and the mass production of high affinity autoreactive antibodies have been shown to occur simultaneously with the development of autoimmune diseases. By the same token this incident is of particular interest and could play a role in the destruction of pancreatic insulin secreting β cells consequently driving the pathogenesis of type I diabetes. Our objective is to identify a possible correlation between the evolution of type I diabetes and the proliferatory behavior of B‐lymphocytes and TFH cells within developing GCs of non‐obese diabetic (NOD) mouse models.