Larman HB, Laserson U, Querol L, Verhaeghen K, Solimini NL, Xu GJ, Klarenbeek PL, Church GM, Hafler DA, Plenge RM, Nigrovic PA, De Jager PL, Weets I, Martens GA, O'Connor KC, et al. *Journal of Autoimmunity* · 2013;43:1–9 · DOI: [10.1016/j.jaut.2013.01.013](https://doi.org/10.1016/j.jaut.2013.01.013) How to cite ### AMA Larman HB, Laserson U, Querol L, et al. PhIP-Seq characterization of autoantibodies from patients with multiple sclerosis, type 1 diabetes and rheumatoid arthritis. *J Autoimmun*. 2013;43:1-9. doi:10.1016/j.jaut.2013.01.013 ### APA ``` Larman, H. B., Laserson, U., Querol, L., Verhaeghen, K., Solimini, N. L., Xu, G. J., Klarenbeek, P. L., Church, G. M., Hafler, D. A., Plenge, R. M., Nigrovic, P. A., De Jager, P. L., Weets, I., Martens, G. A., O'Connor, K. C., et al. (2013). PhIP-Seq characterization of autoantibodies from patients with multiple sclerosis, type 1 diabetes and rheumatoid arthritis. *Journal of Autoimmunity*, 43, 1–9. https://doi.org/10.1016/j.jaut.2013.01.013 ``` ### BibTeX ``` @article{larman2013phipseq, author = {Larman, H. Benjamin and Laserson, Uri and Querol, Luis and Verhaeghen, Katrijn and Solimini, Nicole L. and Xu, George Jing and Klarenbeek, Paul L. and Church, George M. and Hafler, David A. and Plenge, Robert M. and Nigrovic, Peter A. and De Jager, Philip L. and Weets, Ilse and Martens, Geert A. and O'Connor, Kevin C.}, title = {PhIP-Seq characterization of autoantibodies from patients with multiple sclerosis, type 1 diabetes and rheumatoid arthritis}, journal = {Journal of Autoimmunity}, volume = {43}, pages = {1-9}, year = {2013}, doi = {10.1016/j.jaut.2013.01.013} } ``` Across 298 independent antibody repertoires — including type 1 diabetes (T1D), multiple sclerosis (MS), rheumatoid arthritis (RA), and matched controls — the authors built a database of peptide-antibody interactions that captures both common population-level reactivities and disease-associated specificities. The work is a foundational result that established phage immunoprecipitation sequencing as a cross-disease autoantigen discovery tool capable of scaling beyond single-cohort, single-indication studies. [ Read publication at Journal of Autoimmunity ](https://doi.org/10.1016/j.jaut.2013.01.013) In this publication: - Screened 298 independent antibody repertoires (including 73 healthy sera) on a single phage-displayed synthetic human peptidome. - T1D patients displayed a prematurely polyautoreactive phenotype — broader autoreactivity than their matched controls. - The MS cohort (CSF and serum from 63 patients) surfaced both novel antibody-peptide interactions and reactivities consistent with prior literature. - The RA cohort (synovial fluid and serum from 64 patients) revealed novel disease-associated specificities independent of conventional seropositivity status. Autoimmune disease arises when the immune system loses tolerance to the body's own proteins in genetically susceptible individuals. Identifying which self-proteins are being targeted has traditionally required candidate-by-candidate testing, which limits the scale and breadth of discovery. The authors had previously built a phage-displayed synthetic human peptidome — a library that displays short peptide fragments spanning the human proteome on the surface of bacteriophage particles — and validated it on a small set of patients with neurological autoimmunity. This study scales that approach. Using phage immunoprecipitation sequencing (PhIP-Seq), the team screened 298 independent antibody repertoires drawn from healthy donors and from patients across three autoimmune diseases: multiple sclerosis (MS), type 1 diabetes (T1D), and rheumatoid arthritis (RA). For each individual, the assay returns a list of peptide-antibody interactions — an autoantibody fingerprint that includes both reactivities common in the general population and reactivities associated with specific disease states. Three cohort-level findings emerged. T1D patients displayed a prematurely polyautoreactive phenotype — that is, broader autoreactivity than their matched controls. The MS cohort, examined in both cerebrospinal fluid and serum from 63 patients, surfaced both novel antibody-peptide interactions and reactivities consistent with prior literature. The RA cohort, examined in synovial fluid and serum from 64 patients, revealed novel disease-associated specificities that did not depend on the patient's conventional seropositivity status. Together the work demonstrates that proteome-wide autoantibody profiling is feasible at population scale and is informative about both shared and disease-specific autoreactivity. 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