Celiac disease (CD) is an intestinal chronic disorder with multifactorial etiology resulting in small intestinal mucosal injuries and malabsorption. Trigger from gluten and related cereal proteins, HLA-DQ2/DQ8 molecules and autoantibodies to tissue transglutaminase, are essential to precipitate the disease. Genetic, dietary and immunological factors explain geographically regional differences in CD. Specific anchoring sites in DQ2/DQ8 peptide binding motifs show affinity to tTG deamidated peptides of gluten and present to gluten restricted T cells to form celiac lesions. The present article reviews the causes, molecular details of CD development, strategies to control and significance of probiotics in reducing the gluten burden in CD.