The origins of autoimmune disease must be identified to effectively treat these life-threatening syndromes. CNM scientists have pioneered the early development of a combined field of study termed glycoimmunology. Recent research revealed that glycan linkages present on all cells control both innate and adaptive immunity by modulating immune receptor expression and function. In some cases, glycan linkages control the apoptosis of immune cells in reducing disease. In other studies, CNM scientists have discovered a novel mechanism of autoimmune disease resulting from the production of aberrant glycan linkages that induce chronic inflammation, which progresses into syndromes similar to those seen in human autoimmunity. Our findings in this regard were the first to establish a mechanism of autoimmune disease-associated pathology that is independent of hematopoietic and bone marrow-derived cell lineages. These discoveries have provided opportunities to further investigate whether defects in glycan linkages caused by either metabolic or genetic abnormalities are among the origins of various human inflammatory syndromes that develop into chronic and acute autoimmune diseases. Our ongoing work includes studies of human patients in collaboration with hospitals and medical research institutes.