**5. Conclusions**

A diverse array of antibodies has been used to inhibit the T3SS. These Abs bind to proteins of the injectisome including the needle tip, translocon, basal body, and effectors. Transcriptional regulators of the T3SS have also been targeted to prevent the formation of the T3SS, but as they are intracellular targets and require innovative cell-penetrating Abs. These can include entrapping DNA encoding the Ab in intrabodies or attachment of membrane-penetrating proteins to the Ab. Once the Ab has reached its target there are multiple mechanisms it can employ to attenuate virulence or increase the host immune response. In general, these Abs neutralize the effectors, mark the bacterial cell for phagocytes to attack, or mark the infected host cell for ADCC by NK cells. Sometimes Abs adopt more specific mechanisms. For example, when targeting the needle tip or translocon the Ab can physically block the secretion of effectors in a secretion blockade. Several anti-T3SS mAbs have advanced to clinical trials, but none have yet made it to market. As we learn more about how these antibodies function there will undoubtedly be potential for improvement of their therapeutic effects, cost of production, and the ease of their delivery.

**Author Contributions:** Writing—original draft preparation, J.A.H. and A.E.M.; writing—review and editing, J.A.H. and A.E.M. All authors have read and agreed to the published version of the manuscript

**Funding:** This research was funded by startup funds from the School of Pharmacy at Virginia Commonwealth University (VCU). This work was also supported by VCU's CTSA (UL1TR002649 from the National Center for Advancing Translational Sciences) and the CCTR Endowment Fund of Virginia Commonwealth University.

**Acknowledgments:** We thank Heather A. Pendergrass for helpful discussions.

**Conflicts of Interest:** The authors declare no conflict of interest.
