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• The general structure of the type three secretion system. • History and evolution of the bacterial type three secretion system (T3SS) from the flagellar system in Gram-negative bacteria. • Immune evasion strategies employed by the bacteria via utilization of the T3SS to deliver effector proteins into the host. • A detailed description of specific T3SS apparatus and the role of the specific effector proteins in bacterial pathogenesis. • Therapeutic intervention strategies against the bacterial T3SS components to combat bacterial virulence. Various Gram-negative bacteria possess a specialized membrane-bound protein secretion system known as the Type III secretion system (T3SS), which transports the bacterial effector proteins into the host cytosol thereby helping in bacterial pathogenesis. The T3SS has a special needle-like translocon that can sense the contact with the host cell membrane and translocate effectors. The export apparatus of T3SS recognizes these effector proteins bound to chaperones and translocates them into the host cell. Once in the host cell cytoplasm, these effector proteins result in modulation of the host system and promote bacterial localization and infection. Using molecular biology, bioinformatics, genetic techniques, electron microscopic studies, and mathematical modeling, the structure and function of the T3SS and the corresponding effector proteins in various bacteria have been studied. The strategies used by different human pathogenic bacteria to modulate the host system and thereby enhance their virulence mechanism using T3SS have also been well studied. Here we review the history, evolution, and general structure of the T3SS, highlighting the details of its comparison with the flagellar export machinery. Also, this article provides mechanistic details about the common role of T3SS in subversion and manipulation of host cellular processes. Additionally, this review describes specific T3SS apparatus and the role of their specific effectors in bacterial pathogenesis by considering several human and animal pathogenic bacteria. [ABSTRACT FROM AUTHOR]