# Andrew G. Plaut
**Andrew G. Plaut** (also cited as A. G. Plaut) is a physician-scientist in mucosal immunology and microbial pathogenesis, Professor of Medicine at Tufts University School of Medicine and [Tufts Medical Center](https://www.edgepedia.org/tufts-medical-center) in Boston. According to *Neisseria gonorrhoeae and Neisseria meningitidis: Extracellular Enzyme Cleaves Human Immunoglobulin A*, he is known for discovering and characterizing the bacterial enzymes called IgA proteases, which cleave human immunoglobulin A, the principal antibody of mucosal surfaces, and for developing those enzymes as a proposed treatment for [IgA nephropathy](https://www.edgepedia.org/iga-nephropathy), a common cause of kidney failure.[1](https://gsbs.tufts.edu/people/faculty/andrew-plaut) • [2](https://facultyprofiles.tufts.edu/andrew-plaut/professional)
| Fact | Detail |
|---|---|
| Field | Mucosal immunology and microbial pathogenesis[1](https://gsbs.tufts.edu/people/faculty/andrew-plaut) |
| Position | Professor of Medicine, Tufts University School of Medicine and Tufts Medical Center, Boston[2](https://facultyprofiles.tufts.edu/andrew-plaut/professional) |
| Training | MD, Tufts School of Medicine, 1962; BS in Anthropology, Ohio State University[1](https://gsbs.tufts.edu/people/faculty/andrew-plaut) |
| Signature work | 1975 *Science* paper reporting a gonococcal and meningococcal enzyme that cleaves human IgA1[3](https://doi.org/10.1126/science.810892) |
| Company | Co-Founder and Chief Medical Officer, IGAN Biosciences, Inc., from 1 January 2006[2](https://facultyprofiles.tufts.edu/andrew-plaut/professional) |
| Center role | Became Director of the GRASP Center, an NIH-funded digestive diseases research center at Tufts[4](https://www.tuftsmedicine.org/research-clinical-trials/research-institutes-department-research/gastroenterology-research/grasp-center) |
| Patent | IgA1 protease polypeptide agents, application published 10 May 2012, assigned to Tufts Medical Center, Inc.[5](https://www.patentsencyclopedia.com/app/20120114629) |
## Training and career
Plaut earned a BS in [Anthropology](https://www.edgepedia.org/anthropology) from [Ohio State University](https://www.edgepedia.org/ohio-state-university) and his MD from Tufts School of Medicine in 1962.[1](https://gsbs.tufts.edu/people/faculty/andrew-plaut) His research has focused on mucosal immunology and microbial pathogenesis, with an emphasis on bacterial enzymes that proteolytically attack human mucosal IgA antibodies.[1](https://gsbs.tufts.edu/people/faculty/andrew-plaut) He holds the rank of Professor of Medicine at Tufts University School of Medicine, based at Tufts Medical Center in Boston.[2](https://facultyprofiles.tufts.edu/andrew-plaut/professional) He also directs the GRASP Center, one of the digestive diseases research centers in the United States funded by the National Institutes of Health.[4](https://www.tuftsmedicine.org/research-clinical-trials/research-institutes-department-research/gastroenterology-research/grasp-center)
## Representative work
His 1975 paper in *Science*, "*Neisseria gonorrhoeae* and *Neisseria meningitidis*: Extracellular Enzyme Cleaves Human Immunoglobulin A," reported that the two bacteria that infect human mucosal surfaces elaborate a highly specific proteolytic enzyme cleaving the IgA1 subclass of IgA. The susceptible Pro-Thr bond lies in a unique region of the IgA heavy chain; the IgA2 subclass, which lacks this peptide bond, is enzyme resistant.[3](https://doi.org/10.1126/science.810892)
## Microbial IgA proteases: mechanism and significance
IgA proteases are extracellular bacterial enzymes whose only known substrate is human IgA of the IgA1 subclass.[6](https://doi.org/10.1056/nejm197811022991802) In a 1978 *New England Journal of Medicine* research paper, Plaut's laboratory examined clinical isolates of *N. gonorrhoeae*, *N. meningitidis*, and eight non-pathogenic neisserial species. All gonococcal and meningococcal strains were enzyme positive; all non-pathogenic strains were negative, making IgA protease production a laboratory marker that distinguishes pathogenic from harmless Neisseriaceae.[6](https://doi.org/10.1056/nejm197811022991802) Among meningococci, the enzyme occurred both in strains carried harmlessly in the nasopharynx and in strains from systemic infections, so the marker separates species rather than disease states within a species.[6](https://doi.org/10.1056/nejm197811022991802)
A companion 1978 review in the same journal, "Microbial IgA Proteases," framed the biological setting: nearly all disease-producing microorganisms gain their initial foothold on skin, mucous membranes, and other structures in direct contact with the external environment, where IgA dominates the immune defense.[7](https://doi.org/10.1056/nejm197806292982608) Because mucosal immune defense is largely mediated by IgA, the specific link between the enzyme and pathogenic neisseria suggested that it may be involved in neisserial pathogenesis.[6](https://doi.org/10.1056/nejm197811022991802) Mechanistically, IgA1 protease cleaves IgA1 at the hinge region, separating the Fc and Fab fragments of the immunoglobulin, which impairs its Fc-mediated effector response.[8](https://pmc.ncbi.nlm.nih.gov/articles/PMC6625846/) Work published in 1980 showed that meningococci release two distinct IgA proteases: type 1 cleaves the prolyl-seryl bond at position 237-238 of IgA1, and type 2 cleaves the prolyl-threonyl bond two residues amino-terminal to it, with serogroup A strains yielding only type 1 and serogroups X and Y only type 2; both are metal chelator-sensitive neutral proteases.[9](https://doi.org/10.1084/jem.152.5.1442) A related metal-dependent IgA protease had been isolated earlier from *[Streptococcus sanguis](https://www.edgepedia.org/streptococcus-sanguis)*, an oral bacterium, cleaving secretory and serum IgA into Fcα and Fabα fragments.[10](https://doi.org/10.4049/jimmunol.113.1.289)
According to the review itself, Plaut consolidated the field in a 1983 review, "The IgA1 Proteases of Pathogenic Bacteria," in *Annual Review of Microbiology* (Volume 37, pages 603-622).[11](https://doi.org/10.1146/annurev.mi.37.100183.003131) His own 1981 review in *Reviews of Infectious Diseases* stated the open question plainly: these enzymes form a structurally heterogeneous group of neutral endopeptidases secreted by bacteria capable of causing human disease, but the role, if any, of the enzymes in promoting infection by pathogenic *Neisseria*, *Haemophilus*, and *Streptococcus* was not known. The same review noted their practical value as reagents, because cleaving IgA with them yields intact Fcα and Fabα fragments.[12](https://doi.org/10.1093/clinids/3.3.521)
## Later research and applications
Plaut's Tufts laboratory now works on IgA nephropathy (Berger's disease), the most common form of glomerulonephritis worldwide and a principal cause of kidney failure.[16](https://pubmed.ncbi.nlm.nih.gov/11062479/) The laboratory is developing bacterial IgA proteases as a treatment intended to reverse the kidney inflammation that leads to kidney failure.[13](https://www.tuftsmedicine.org/research-clinical-trials/research-institutes-department-research/gastroenterology-research/andrew-plaut-md-laboratory) In laboratory work described by Tufts Clinical and Translational Science Institute, the team used intravenous injections of *Haemophilus influenzae* IgA protease to remove human IgA1 deposits introduced into mouse kidneys, and, according to the Tufts Clinical and Translational Science Institute, collaborated with BioMarin Pharmaceutical, a California pharmaceutical company, to produce and later modify the *Haemophilus* IgA protease structure for human injection. A patent for this enzyme-based approach to treating IgA nephropathy was sought and issued to Tufts Medical Center.[14](https://igan.org/wp-content/uploads/2015/10/Tufts_Enzymes.pdf) Patent application 20120114629, published 10 May 2012, covering IgA1 protease polypeptide agents, names Tufts Medical Center, Inc. as assignee.[5](https://www.patentsencyclopedia.com/app/20120114629)
Plaut has also been Co-Founder and Chief Medical Officer of IGAN Biosciences, Inc. since 1 January 2006.[2](https://facultyprofiles.tufts.edu/andrew-plaut/professional) Separately, he collaborated with a Tufts Department of Biochemistry researcher in developing DPPIV inhibitory drugs now used to treat Type II diabetes.[13](https://www.tuftsmedicine.org/research-clinical-trials/research-institutes-department-research/gastroenterology-research/andrew-plaut-md-laboratory)
## Status as of 2026
Tufts records show Plaut teaching an introductory infectious-disease course from 1 July to 23 August 2024 and again from 1 July to 22 August 2025.[15](https://facultyprofiles.tufts.edu/andrew-plaut/teaching) He states that he no longer accepts dissertation students but remains an active participant in teaching and program activities.[1](https://gsbs.tufts.edu/people/faculty/andrew-plaut) He remains active in studying IgA deposition diseases, which he describes as a common cause of renal failure that his group proposes to reverse by using bacterial IgA proteases for treatment of patients.[1](https://gsbs.tufts.edu/people/faculty/andrew-plaut)
## References
1. [Andrew Plaut | Graduate School of Biomedical Sciences, Tufts University](https://gsbs.tufts.edu/people/faculty/andrew-plaut)
2. [Andrew Plaut, M.D. Professional Activities | Tufts University](https://facultyprofiles.tufts.edu/andrew-plaut/professional)
3. [*Neisseria gonorrhoeae* and *Neisseria meningitidis*: Extracellular Enzyme Cleaves Human Immunoglobulin A, Science, 1975](https://doi.org/10.1126/science.810892)
4. [GRASP Center | Tufts Medicine](https://www.tuftsmedicine.org/research-clinical-trials/research-institutes-department-research/gastroenterology-research/grasp-center)
5. [IgA1 protease polypeptide agents and uses thereof, Patent application 20120114629](https://www.patentsencyclopedia.com/app/20120114629)
6. [IgA Protease Production as a Characteristic Distinguishing Pathogenic from Harmless Neisseriaceae, New England Journal of Medicine, 1978](https://doi.org/10.1056/nejm197811022991802)
7. [Microbial IgA Proteases, New England Journal of Medicine, 1978](https://doi.org/10.1056/nejm197806292982608)
8. [Small-molecule inhibitors of Haemophilus influenzae IgA1 protease (PMC)](https://pmc.ncbi.nlm.nih.gov/articles/PMC6625846/)
9. [IgA proteases of two distinct specificities are released by Neisseria meningitidis, Journal of Experimental Medicine, 1980](https://doi.org/10.1084/jem.152.5.1442)
10. [Isolation of an Enzyme from Streptococcus Sanguis Which Specifically Cleaves IgA, Journal of Immunology, 1974](https://doi.org/10.4049/jimmunol.113.1.289)
11. [The IgA1 Proteases of Pathogenic Bacteria, Annual Review of Microbiology, 1983](https://doi.org/10.1146/annurev.mi.37.100183.003131)
12. [Secretory Immunity and the Bacterial IgA Proteases, Reviews of Infectious Diseases, 1981](https://doi.org/10.1093/clinids/3.3.521)
13. [Andrew Plaut, MD Laboratory | Tufts Medical Center](https://www.tuftsmedicine.org/research-clinical-trials/research-institutes-department-research/gastroenterology-research/andrew-plaut-md-laboratory)
14. [Using Enzymes to Reverse Kidney Disease | Tufts Clinical and Translational Science Institute](https://igan.org/wp-content/uploads/2015/10/Tufts_Enzymes.pdf)
15. [Andrew Plaut, M.D. Teaching Activities | Tufts University](https://facultyprofiles.tufts.edu/andrew-plaut/teaching)
16. [pubmed.ncbi.nlm.nih.gov](https://pubmed.ncbi.nlm.nih.gov/11062479/)
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*Topic: Encyclopedia › Life and health › Life and health scientists › Medical and health researchers › Immunology and allergy researchers › Infection and vaccine immunity researchers*
*Initially written Sep 21, 2026 · Reviewed: Sep 25, 2026; Sep 30, 2026 · Edited: Sep 25, 2026; Sep 30, 2026 · Last review: Sep 30, 2026*
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