Soyeon Kim

All Publications

• CXCR6+CD127- Tr1 cells balance immunity and persistence in Plasmodium falciparum infection. The Journal of clinical investigation Nideffer, J., Bach, F., Strubbe, S., Lopez, L., Zedi, M., Nankya, F., Briggs, J., van der Ploeg, K., Musinguzi, K., Kim, S., Garcia Romero, A., Keya, A., Camanag, K., Lewis, S., Abdelbasset, M., Wang, B., Boss, A., Nansubuga, E., Nankabirwa, J. I., Arinaitwe, E., Takahashi, S., Dorsey, G., Greenhouse, B., Rodriguez-Barraquer, I., Kamya, M. R., Bacchetta, R., Ssewanyana, I., Haque, A., Roncarolo, M. G., Jagannathan, P. 2026

  Abstract

  Plasmodium falciparum (Pf) induces the clonal expansion of antigen-specific type 1 regulatory T (Tr1) cells capable of long-term memory. Tr1 cells comprise nearly 90% of the Pf blood stage antigen-specific CD4+ T cell pool in children. Though, whether Tr1 cells contribute to protection from malaria remains undetermined. To address this critical knowledge gap, we first performed scRNA-seq on gated cell populations and validated CXCR6+ CD127- as new phenotypic markers to enrich for bona-fide Tr1 cells. Importantly, these Tr1 cells potently suppressed the proliferation of other CD4+ T cells in vitro via IL-10 secretion. Among children living in malaria-endemic Uganda, CXCR6+ CD127- Tr1 cells were the dominant responding subset to Pf-infected red blood cell stimulation in vitro. They also rapidly expanded following malaria and expressed IL-10 and IFNγ during infection in vivo. Tr1 abundance correlated with plasma concentrations of granzyme A, IFNγ, IL-10, and LAG3, suggesting that these cells act systemically. Higher CXCR6+ CD127- Tr1 cell frequencies correlated with a lower probability of symptoms given parasitemia but were also associated with delayed parasite clearance among untreated, asymptomatic children. These data suggest that Tr1 cells help mediate clinical immunity to malaria but may also facilitate parasite persistence through mechanisms of immune regulation.

  View details for DOI 10.1172/JCI200628

  View details for PubMedID 42084919

• Clone tracking through repeated malaria identifies high-fidelity memory CD4 T cell responses. Science immunology Nideffer, J., Bach, F., Nankya, F., Musinguzi, K., Borna, Š., Mantilla, M., Zedi, M., Garcia Romero, A., Gerungan, C., Yang, N., Kim, S., van der Ploeg, K., Camanag, K., Lopez, L., Nansubuga, E., Nankabirwa, J. I., Arinaitwe, E., Boonrat, P., Strubbe, S., Cepika, A. M., Takahashi, S., Dorsey, G., Greenhouse, B., Rodriguez-Barraquer, I., Kamya, M. R., Bacchetta, R., Ssewanyana, I., Haque, A., Roncarolo, M. G., Jagannathan, P. 2025; 10 (106): eads2957

  Abstract

  Few studies have tracked human CD4+ T cell clones through repeated infections. We used longitudinal single-cell RNA and T cell receptor (TCR) tracking to study the functional stability and memory potential of CD4+ T cell clonotypes during repeated Plasmodium falciparum (Pf) infections in Ugandan children and adults. Nearly all clonotypes displayed a strong preference for one of seven CD4+ subsets. This phenomenon of "clonal fidelity" was influenced by clonal expansion, linking T cell polarization and proliferation in vivo. Using clone tracking, we characterized subset-specific activation trajectories and identified antigen-specific clones. Type 1 regulatory T (TR1) cells accounted for nearly 90% of Pf-specific CD4+ T cells in blood. Tracking these clones longitudinally for hundreds of days, we observed malaria-induced expansion of TR1 effectors, long-term persistence of TR1 memory cells, and high-fidelity recall responses after reinfection. This work establishes clonal fidelity as a natural phenomenon and demonstrates the stable, long-term memory potential of TR1 cells.

  View details for DOI 10.1126/sciimmunol.ads2957

  View details for PubMedID 40279404

• Everlasting first impressions in B cells. Science immunology Kim, S., Maltzman, J. S. 2024; 9 (95): eadq0015

  Abstract

  Initial imprinting by type 1 interferons shapes memory B cell generation in chronic viral infection.

  View details for DOI 10.1126/sciimmunol.adq0015

  View details for PubMedID 38701192

• Defective N-glycosylation in tumor-infiltrating CD8(+) T cells impairs IFN-?-mediated effector function IMMUNOLOGY AND CELL BIOLOGY Kim, S., Min, H., Nah, J., Jeong, J., Park, K., Kim, W., Lee, Y., Kim, J., An, J., Seong, R. 2023; 101 (7): 610-624

  Abstract

  T cell-mediated antitumor immunity is modulated, in part, by N-glycosylation. However, the interplay between N-glycosylation and the loss of effector function in exhausted T cells has not yet been fully investigated. Here, we delineated the impact of N-glycosylation on the exhaustion of tumor-infiltrating lymphocytes in a murine colon adenocarcinoma model, focusing on the IFN-γ-mediated immune response. We found that exhausted CD8+ T cells downregulated the oligosaccharyltransferase complex, which is indispensable for N-glycan transfer. Concordant N-glycosylation deficiency in tumor-infiltrating lymphocytes leads to loss of antitumor immunity. Complementing the oligosaccharyltransferase complex restored IFN-γ production and alleviated CD8+ T cell exhaustion, resulting in reduced tumor growth. Thus, aberrant glycosylation induced in the tumor microenvironment incapacitates effector CD8+ T cells. Our findings provide insights into CD8+ T cell exhaustion by incorporating N-glycosylation to understand the characteristic loss of IFN-γ, opening new opportunities to amend the glycosylation status in cancer immunotherapies.

  View details for DOI 10.1111/imcb.12647

  View details for Web of Science ID 000980081000001

  View details for PubMedID 37114567