Shigella invasion plasmid antigen D (IpaD) (IpaD)

Shigella invasion plasmid antigen D (IpaD) is a pivotal component of the Type III Secretion System (T3SS) in Shigella species, which are responsible for bacillary dysentery (UniProt P18013) [20]. Positioned at the distal tip of the T3SS needle, IpaD functions as a regulatory "plug" that controls the secretion of effector proteins and acts as a sensor for host environmental cues, such as bile salts (Barta et al., 2017) [1]. Upon activation, IpaD undergoes conformational changes that facilitate the recruitment of translocator proteins IpaB and IpaC to form a pore in the host cell membrane, enabling the injection of virulence factors into the host cytoplasm (Dickenson et al., 2011) [31]. Because of its essential role in bacterial entry and its high conservation across Shigella serotypes, IpaD is a major target for the development of vaccines, monoclonal antibodies, and small-molecule inhibitors designed to block the infection process (Li et al., 2024) [2]. Therapeutic strategies targeting IpaD aim to prevent the formation of the translocon pore, thereby neutralizing the pathogen's ability to invade host cells and cause disease (Ebrahimizadeh et al., 2021) [5]. Current research focuses on identifying functional epitopes for vaccine design and developing high-affinity antibodies or small molecules that can disrupt the T3SS assembly or function (Barta et al., 2017; Li et al., 2024) [1, 2].

Other names

Invasin IpaD36 kDa membrane antigenSctAipaD

Inhibition of the Type III secretion system (T3SS) needle tip function, preventing host cell sensing and translocon pore formation.