The origins of autoimmune disease must be identified to prevent and effectively treat these life-threatening syndromes. CNM scientists have co-pioneered the early development of a combined field of study termed glycoimmunology. This field reflects research discoveries that have revealed that glycosidic linkages commonly present on most secreted proteins control both innate and adaptive immunity by modulating immune receptor expression and function. In some cases, such glycan modifications control the apoptosis of immune cells in modulating disease. In related studies, our scientists identified a novel mechanism of disease that may explain how some autoimmune syndromes originate. This mechanism is initiated by the presence of aberrant glycan linkages among somatic and non-hematopoietic cell types that induce a sterile and chronic inflammation, which progresses into signs similar to those seen in human autoimmune disease including lupus erythematosus. These findings established an unexpected disease mechanism with tissue destruction that is independent of adaptive immune function. Our scientists are further investigating whether defects in glycan structures caused by metabolic and possibly overlapping genetic abnormalities are among the mysterious origins of autoimmune disease. Our research includes studies of human patient blood samples in collaboration with hospitals and medical research institutes.