8 Pathology Multiple sclerosis Type 1 diabetes Table 3: Mitochondrial dynamics and neuroinﬂammatory and autoimmune diseases. Proteins involved Mitochondrial (expression level and/or mutation) phenotype OPA1 mutation OPA1 ↓↓ DRP1 ↑↑ PHBs mutation Fragmentation. Fragmentation, disruption of cristae structure. International Journal of Cell Biology Mechanisms of pathophysiology involving mitochondria Reduction of respiratory rates with lower ATP production [139, 140]. Alteration in OPA1 processing in β-cells in the pancreas and coronary endothelial cells from diabetic animals [141, 142]. fragment and relocalize at the immunological synapse in close proximity to the plasma membrane to buﬀer Ca2+ entrance and to avoid calcium-dependent T-cell inactivation [147]. Moreover, upon activation, T cells migrate to the site of inﬂammation towards a chemoattractant gradient. Our group reported that mitochondria allow lymphocyte migration by relocating and accumulating at the uropod (the posterior area of an activated T cell) where they can provide the necessary energy to class II myosin proteins, these being the major cellular motors. Interestingly, this reorganization needs mitochondrial ﬁssion while a forced fusion inhibits both mitochondrial relocalization and lym- phocyte migration [45]. In recent years, the polarization of mitochondria towards cell-cell surface has also been shown to occur between natural killer (NK) and tumoral cells [148, 149]. Mitochondrial ﬁssion, driven by FIS1 and DRP1, also contributes to the immune system tolerance and the tumor- immune escape in a galectin-1 (GAL-1)-dependent manner. GAL-1 sensitizes resting and activated T cells to FAS- mediated cell death program, which is characterized by mitochondrial dysfunctions, membrane potential alteration, mitochondrial ﬁssion, and cytochrome c release [150]. It still remains to be elucidated whether or not mito- chondrial dynamics play a crucial role in other important physiological processes in T cells. Finally, CD47 can trigger cell death in a B lymphocyte leukemia. Also this apoptotic pathway is characterized by DRP1 translocation to mitochondria, which depends on chymotrypsin-like proteases, Δψ loss and ROS production [151]. This last observation is an indication of a possible role of mitochondrial dynamics in general in the whole immune system, more than only in the T-cell physiology and pathophysiology. 5. Conclusion The observations here presented suggest a prominent role for mitochondrial dynamics in a plethora of pathways from cell proliferation to resistance to apoptosis, from cell- energetic requirements to quality control mechanisms, from homeostasis to activation and movement of immune system cells. However our observations also suggest the potential for many new ﬁndings to come. 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