The blood–brain barrier (BBB), an anatomically and functionally unique structure, maintains the homeostasis of the central nervous system (CNS) by maintaining the optimal ionic environment for neuronal function and transporting trophins or nutrients, as well as restricting access of toxic substances, inflammatory cells, circulating antibodies, and pathogens under physiological and pathological conditions. Brain microvascular endothelial cells directly mediate BBB function. Along with a battery of efflux transporters, the tight junctions of brain microvascular endothelial cells form the anatomical and functional basis of the barrier function of the BBB. Access to the CNS by inflammatory cells is restricted, but not prohibited. Transendothelial migration through the BBB is characterized by tightly controlled multi‐step processes. BBB dysfunction in neurological autoimmune diseases is associated with autoreactive and inflammatory cells and autoantibodies that invade the CNS and induce neuroinflammation. It is still incompletely understood how these neuro‐invaders affect the BBB and gain entry into the CNS across the BBB. In the present review, we introduce current knowledge of BBB cellular components and the multistep process of inflammatory cells crossing the BBB in physiological conditions, and summarize their biological mechanisms to cross the BBB in pathological conditions in representative neurological autoimmune diseases (multiple sclerosis, neuromyelitis optica and systemic lupus erythematosus) with a particular focus on new and recent findings.