Search bioRxiv⌕ Search

bioRxiv · 10.1101/2025.09.05.665822

Protective immunity against malaria by a nanoparticle CIS43-based junctional vaccine alone or in combination with R21

Abstract

Repetitive display of the major repeats of the Plasmodium falciparum circumsporozoite protein (PfCSP) is the basis for two WHO-recommended vaccines: RTS,S/AS01 and R21/Matrix-M. Recently, however, the CIS43 monoclonal antibody that preferentially targets the junctional region of PfCSP has been shown to be highly protective in humans, highlighting its junctional epitope as a key vaccine target. Here, we develop a vaccine based on the tandem repeats of the junctional epitope displayed on a self-assembling nanoparticle, and compare this CIS43-based junctional vaccine alone or in combination with the benchmark R21 vaccine, using both B cell analysis and monoclonal antibody isolation to define targeting of the immune response. Comparable reduction in liver burden was observed following vaccination with junctional and R21 vaccines at a dose of 1 g. At a dose of 0.25 g, a modest reduction of malaria-liver burden with the junctional vaccine was observed compared to R21. Further, combining junctional and R21 vaccines induced modestly enhanced protection compared to either vaccine alone. While the R21 vaccine elicited antibodies primarily against the major repeats, the junctional vaccine elicited antibodies against both junctional and major repeat regions. In vivo-B cell analysis and isolation of monoclonal antibodies confirmed differences in vaccine-induced antibody specificities. Altogether, these data suggest the nanoparticle-formatted tandem-repeated CIS43-junctional vaccine to be a promising approach to broaden immunity against malaria, either as a standalone intervention or in combination with R21. HIGHLIGHTSO_LIDeveloped a self-assembling nanoparticle-displayed junctional vaccine of PfCSP based on tandem repeats of the epitope preferentially targeted by the highly protective CIS43 antibody C_LIO_LIThe CIS43-based junctional vaccine at low doses significantly reduced liver burden following malaria challenge in mice C_LIO_LIFollowing either low or high doses of the junctional vaccine in naive mice, adoptively transferred B cells expressing the CIS43 inferred germline sequence yielded a high frequency of germinal center and ASC responses C_LIO_LIThe CIS43-based junctional vaccine elicits antibodies against junctional and major repeat regions whereas the R21 vaccine elicits responses primarily against the major repeat region C_LIO_LIAt low dose, the CIS43-based junctional vaccine given together with the R21 vaccine showed modestly improved control of liver burden compared to either vaccine alone C_LI

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Tripathi, P., Koo, J.-H., Chen, X., Da Silva Pereira, L., Dillon, M., Zhang, B., Lofgren, M., Nguyen, K. T., Teng, I.-T., Bonilla, B., Kerscher, S., Kong, W.-P., Ransier, A., Stephens, T., Tsybovsky, Y., Weldon, S. R., Douek, D. C., Pierson, T. C., Batista, F. D., Idris, A. H., Seder, R. A., Kwong, P. D., Zhou, T.. 2025-09-08. Protective immunity against malaria by a nanoparticle CIS43-based junctional vaccine alone or in combination with R21. https://doi.org/10.1101/2025.09.05.665822

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

TFAM Dependent Mitochondrial Fitness Limits CD8⁺ T Cell Immunopathology and Sustains Protective Immunity during Viral Pneumonia

During respiratory virus infection, CD8 T cells kill infected cells and establish antigen-specific memory, but mechanisms regulating these functions remain incompletely understood. Here, we identify mitochondrial transcription factor A (TFAM)-dependent mitochondrial fitness as a regulator of CD8 T cell function during influenza infection. Human CD8 T cells exhibited an age-associated decline in TFAM expression and mitochondrial function. To model this physiologically relevant decline and determine its consequences for antiviral immunity, we generated CD8 T cell-specific TFAM-haploinsufficient mice. TFAM insufficiency disrupted mitochondrial integrity and bioenergetics and increased mitochondrial DNA and oxidative stress. During influenza infection, TFAM-insufficient CD8 T cells exhibited increased cytotoxic and inflammatory activity associated with lung immunopathology without improved viral control. This early phenotype was followed by loss of effector function, diminished antigen-specific responses, reduced protection following adoptive transfer, and impaired heterosubtypic recall immunity. Thus, TFAM-dependent mitochondrial fitness is a cell-intrinsic regulator that limits immunopathology while sustaining recall immunity.

immunology↗

Gasdermin E couples mitochondrial stress to STING-driven neuronal pyroptosis during Chandipura virus encephalitis

Neurotropic RNA viruses are major causes of fatal encephalitis worldwide, yet how infected neurons transition from antiviral defense to inflammatory cell death is not well characterized. Chandipura virus (CHPV), an emerging neurotropic rhabdovirus, causes acute, rapidly progressive encephalitis with high case fatality in children, but the mechanisms underlying its neuropathogenesis remain poorly defined. Here, we demonstrate that CHPV suppresses canonical RNA virus sensing early but subsequently switches to a mitochondria-driven innate immune program that culminates in inflammatory cell death. Early infection of neuronal cells with CHPV was marked by reduced levels of the mitochondrial antiviral adaptor protein, MAVS and attenuation of type I and III interferon responses. As infection progressed, mitochondrial dysfunction promoted accumulation of mtROS, mitochondrial accumulation of cleaved GSDME and cytosolic mtDNA release, triggering STING activation, which coincided with robust neuroinflammation and pyroptotic cell death. Pharmacological inhibition or genetic silencing of STING markedly attenuated inflammatory signaling, prevented pyroptotic membrane rupture and protected neurons from cell death without significantly affecting viral replication. In contrast, GSDME depletion reduced both viral replication and neuronal death. Notably, GSDME depletion markedly attenuated STING phosphorylation, while STING depletion also reduced GSDME activation, revealing functional coupling between these pathways during CHPV-induced neuronal injury. Collectively, our findings identify a mitochondria-GSDME-STING axis linking early immune evasion to neuroinflammation during CHPV infection, revealing a previously unrecognized mechanism of inflammatory neuronal death in viral encephalitis and highlighting STING as a potential therapeutic target in certain CNS viral infections.

immunology↗

Mutanome-guided immunopeptidomics of blood plasma for neoepitope detection in solid tumors is constrained by cfDNA variant calling sensitivity and MS detection limits

Introduction: Neoepitopes form the basis of tumor-specific immune responses. Tissue biopsy, the primary source for neoepitope detection, is limited and invasive. Therefore, we aimed to identify neoepitopes by mutanome-guided immunopeptidomics from plasma of cancer patients. Methods: Mass spectrometry (MS) data analysis of HLA ligands from plasma (n = 4) was guided by patient-specific mutanomes of cell-free DNA (cfDNA) from plasma or tumor genomic DNA (tgDNA) from tissue. Matched tumor tissue and healthy donor plasma served as controls. Neoepitopes were validated with synthetic peptides, and immunogenicity was assessed using IFN-gamma ELISpot and intracellular cytokine staining. Results: Wild-type immunopeptidomes from tissue and plasma overlapped by 58%, with 91% of plasma HLA ligands rediscovered in tissue. 13 out of 15 tumor-associated HLA ligands detected in plasma were rediscovered in the matching tissue. However, no neoepitopes in plasma were identified by immunopeptidomics guided by cfDNA mutanomes, likely reflecting the limited overlap between cfDNA and tgDNA mutanomes (15%). Using the tgDNA mutanome as a complementary reference, two neoepitopes were detected in one patient's plasma, albeit at the MS detection limit. Both neoepitopes were also discovered in tissue, along with three tissue-exclusive neoepitopes. Two tissue-exclusive neoepitopes induced antigen-specific T cell responses in healthy donor PBMCs. Conclusion: In summary, plasma immunopeptidomics enables profiling of HLA ligands from wild-type proteins, including TAAs. In principle, neoepitope detection from plasma at the peptide level is feasible, but tissue remains the gold standard for variant calling and neoepitope identification. Improved detection methods may enable minimally invasive approaches in the future.

immunology↗