Galectins are a class of proteins that bind specifically to β-galactoside sugars, such as N-acetyllactosamine which can be bound to proteins by either N-linked or O-linked glycosylation. They are also termed S-type lectins due to their dependency on disulphide bonds for stability and carbohydrate binding. Mammalian galectins have either one or two highly conserved carbohydrate recognition domains (CRDs) to form complexes that crosslink glycosylated ligands. Gal-3 is important in numerous biological activities in various organs, including cell proliferation, apoptotic regulation, inflammation, fibrosis, and host defense. The presence of Gal-3 has been demonstrated also in the tissues of the lungs, spleen, stomach, and also in the heart, kidneys, pancreas, and liver. Thus, a significant increase of Gal-3 level in the blood serum is observed in many pathological processes which take place in various tissues. Gal-3 affects differentiation and growth of various immune cells: it induces apoptosis in T cells and neutrophils; and it activates several lymphoid and myeloid cells resulting in mediator release, superoxide anion production, and cytokine production. Notably, Gal-3 induces monocyte–macrophage differentiation, interferes with dendritic cell fate decision, regulates apoptosis on T lymphocytes and inhibits B-lymphocyte differentiation into immunoglobulin secreting plasma cells. Considering the influence of these cell populations in the pathogenesis of several autoimmune diseases, Gal-3 seems to play a role in development of autoimmunity. Many studies have revealed that Gal-3 plays an important role as a diagnostic or prognostic biomarker for certain types of heart disease, kidney disease, viral infection, autoimmune disease, neurodegenerative disorders, and tumor formation. In particular for detecting many of these diseases in their early stages.