Humoral Dynamics and Autoimmunity Laboratory

Dr Ding’s research focuses on the regulation of B-cell and plasma-cell fates, and on how these cells interact with other immune populations in both homeostasis and antibody-mediated autoimmune disease, particularly emphasising on neuro-autoimmune conditions such as autoimmune encephalitis. The Humoral Dynamics and Autoimmunity Laboratory investigates the fundamental mechanisms that govern immune dynamics across tissues—including within the central nervous system—with the goal of translating these discoveries into clinically actionable biomarkers and targeted therapies that improve disease outcomes.

Our research

The research work in our lab centres on a program that integrates three interconnected pillars: humoral immunity, neuroimmune regulation and immune tolerance (HINT). We investigate the fundamental mechanisms that shape antibody-mediated immunity across tissues, with a particular focus on how dysregulated humoral responses contribute to autoimmune and neurological disorders. The HINT program encompasses humoral immunity—examining B-cell and plasma-cell fate decision, longevity and repertoire dynamics; neuroimmune regulation—defining how immune circuits operate within the central nervous system and its barrier interfaces; and immune tolerance—uncovering how certain risk factors contributes to the breakdown of immune tolerance and lead to pathogenic antibody responses. Together, these themes provide a mechanistic framework for understanding how humoral immunity becomes dysregulated in conditions such as autoimmune encephalitis and other antibody-mediated disorders. The overarching goal of HINT is to translate these mechanistic insights into biomarkers and targeted therapeutic strategies that improve diagnosis, monitoring and treatment outcomes for patients with autoimmune and neurological disorders.

Our people

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Selected publications

  • Mulder J., Scrofani J., Chheng K., O’Donnell K., Tarlinton D.M., Robinson M.J.#, Ding Z.#. Examining the Conditions Associated with Establishing Plasma Cell Persistence. J Immunol. 2025. 214(8):2112-2123.
  • Ding Z., Dowling M.R., Wade-Vallance A.K., Dvorscek A.R., Pitt C., Mulder J., O'Donnell K., McKenzie C., Karaviotis A.B., Scrofani J., Perdijk O., Hill D.L., Quast I., Tarlinton D.M., Allen C.D.C., Robinson M.J.. Long-lived IgE plasma cells persist in secondary lymphoid tissues using a navitoclax-sensitive survival program. Immunity. 2025. 58(11):2704-2716.e4.
  • Ding Z.*#, Hagan M.*, Yan F., Schroer N.W.Y, Polmear J., Good-Jacobson K.L., Dvorscek A.R., Pitt C., O'Donnell K., Nutt S.L., Zotos D., McKenzie C., Hill D.L., Robinson M.J., Quast I., Koentgen F., Tarlinton D.M.# Ki67 deficiency impedes chromatin accessibility and BCR gene rearrangement. J Exp Med. 2024. 221(8):e20232160.
  • Robinson M.J.*, Ding Z.*, Dowling M.R., Hill D.L., Webster R.H., McKenzie C., Pitt C., O’Donnell K., Mulder J., Brodie E., Hodgkin P.D., Wong N.C., Quast I., Tarlinton D.M. Intrinsically driven turnover underlies broad plasma-cell lifespan heterogeneity. Immunity. 2023. 56(7):1596-1612.e4.