Autoimmune and neuroinflammatory diseases arise from complex and sustained disturbances in immune regulation rather than from isolated cellular defects. Increasing evidence indicates that pathological outcomes in these conditions are driven by aberrant communication networks among immune cells operating across peripheral tissues, the central nervous system, and immune–privileged compartments. Immune cell crosstalk governs antigen recognition, cytokine amplification, tissue infiltration, and resolution of inflammation, and its dysregulation leads to chronic immune activation, loss of tolerance, and progressive tissue damage. This short communication synthesizes current understanding of immune cell–cell interactions as a unifying mechanistic framework underlying autoimmune and neuroinflammatory disorders. Emphasis is placed on bidirectional signaling between innate and adaptive immune populations, the role of cytokine and chemokine circuits, and the influence of tissue-specific microenvironments on immune behavior. Practical implications for disease monitoring and therapeutic intervention are discussed, highlighting how targeting immune communication networks rather than single cell types may provide more durable clinical benefit. By integrating mechanistic insights with translational perspectives, this work underscores immune crosstalk as a central determinant of disease initiation, propagation, and therapeutic responsiveness.