About

Avery August, PhD, is a Professor of Immunology, HHMI Professor, and Deputy Provost at Cornell University College of Veterinary Medicine. He previously served as a Distinguished Professor of Immunology in the Department of Veterinary & Biomedical Sciences and was the Director of the Center for Molecular Immunology & Infectious Disease at The Pennsylvania State University at University Park. Dr. August holds a B.S. degree in Medical Technology from California State University at Los Angeles and a Ph.D. in Immunology from the Weill Cornell Graduate School of Medical Sciences. He was a Postdoctoral fellow at The Rockefeller University. His research focuses on the regulation of immune responses by intracellular signaling events, particularly the role of Tyrosine Kinases (TKs), including the Tec family of non-receptor TKs, in immune cell development and function. His work investigates how Tec family kinases, such as Itk, influence T-cell development, differentiation, and cytokine production, with applications in understanding inflammatory and infectious diseases. Dr. August's studies utilize mouse models of lung and mucosal inflammatory and infectious diseases, including flu, allergic asthma, and inflammatory bowel disease, to explore these signaling pathways. He has shown that the absence of Itk enhances CD8+ T cell memory development, especially innate memory T cells dependent on IL4, which can respond rapidly to infections. His research aims to elucidate the molecular mechanisms driving T cell differentiation, cytokine regulation, and immune memory formation.

Research topics

• Biology
• Sociology
• Social Science
• Biochemistry
• Environmental ethics
• Immunology
• Gender studies
• Cell biology
• Engineering ethics
• Chemistry
• Medicine
• Virology

Selected publications

• Diverse microbial exposure exacerbates the development of allergic airway inflammation in adult mice

  The Journal of Immunology · 2026-02-01

  articleOpen accessSenior author

  Exposure to a diversity of microbes has been implicated in playing a major role in susceptibility to the development of allergic lung-type diseases. The hygiene hypothesis suggests that those exposed to a broad diversity of microbes are more likely to be protected against developing allergic-type diseases. However, changes in exposure to microbial diversity can occur in both younger individuals, as well as in adults, and the effects are not always understood. We investigated the effect of exposure to broad microbial diversity on the airway T cell response in house dust mite-induced allergic airway disease (a model of allergic asthma) in mice. We increased exposure to broad microbial diversity by cohousing specific pathogen-free adult or newborn mice with pet store mice (pet store exposure or born in pet store exposed, respectively). Mice were then exposed to house dust mite to induce allergic airway disease. Our findings suggest an effect of increased microbial exposure on the development of allergic airway inflammation that differs by age. Increasing exposure to diverse microbes as adults likely exacerbates the development of allergic airway inflammation, whereas this was not observed when exposure occurred at birth. We suggest that experimental evaluation of the hygiene hypothesis in inflammation, particularly those using mouse models, may need to consider age of the host and time of microbial exposure.

  PublisherDOI

• Sulfur-containing class of broad-spectrum antivirals improves influenza virus vaccine development

  Nature Communications · 2026-01-06

  articleOpen access

  Enveloped viruses are significant zoonotic disease threats with the potential to cause global pandemics. We identified a class of small-molecule sulfur-containing antiviral compounds (XM series) that broadly inhibit enveloped viruses. Multidisciplinary approaches revealed that XM compounds alter the viral membrane lipid chemical composition, enhance membrane order within the hydrophobic bilayer, and increase membrane phase transition temperatures. This mechanism inhibits membrane fusion and viral entry, while leaving the viral glycoproteins and genomes largely unaffected. Leveraging these unique properties, we develop a proof-of-concept whole inactivated influenza virus (IIV) vaccine using XM-01 (XM-01-IIV). In a mouse model, XM-01-IIV elicit significantly enhanced neutralizing antibody responses against hemagglutinin and neuraminidase compared to traditional paraformaldehyde-inactivated vaccines. Further, XM-01-IIV reduces morbidity and mortality following influenza challenge, achieving protection comparable to live virus vaccination. This promising class of broadly acting antivirals can be highly impactful in the development of highly potent inactivated vaccines for enveloped viruses.

  PublisherOA PDFDOI

• Programming immunogenicity of dengue EDIII vaccine antigens using engineered outer membrane vesicles (OMVs)

  Vaccine X · 2025-06-19 · 3 citations

  articleOpen access

  Dengue is a mosquito-borne viral infection and is more prevalent in the world with no therapeutics and suboptimal vaccine (Dengvaxia) performance against all four serotypes of the dengue virus. Hence, there is an urgent requirement for a non-infectious and non-replicative vaccine candidate that can elicit a balanced and serotype-specific immune response. In this study, we have engineered bacterial outer membrane vesicles (rOMVs) that display EDIII antigens (EDIII rOMVs). The current formulation modulates the expression of costimulatory molecules on antigen-presenting cells (APCs) as well as enhances the uptake and presentation. Subsequently, the EDIII rOMVs elicited a strong antigen-specific polyfunctional response from CD4+ and CD8 + T cells. The robust antibody response was facilitated by a germinal center reaction characterized by high T follicular helper (Tfh) and B cell response levels in the mice that received EDIII rOMVs. Notably, the produced antibodies demonstrated the ability to neutralize all four dengue virus serotypes in an in vitro infection model, indicating its potential role in protective immunity.

  PublisherDOI

• Diverse microbial exposure exacerbates the development of allergic airway inflammation in adult mice

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-25

  preprintOpen accessSenior authorCorresponding

  Background: Exposure to a diversity of microbes has been implicated in playing a major role in susceptibility to the development of allergic lung type diseases. The hygiene hypothesis suggests that those exposed to a broad diversity of microbes are more likely to be protected against developing allergic type diseases. However, changes in exposure to microbial diversity can occur in both younger individuals, as well as in adults, and the effects are not always understood. Objective: We investigated the effect of exposure to broad microbial diversity on the airway T cell response in house dust mite (HDM) induced allergic airway disease (AAD, a model of allergic asthma). Methods: We increased exposure to broad microbial diversity by co-housing specific pathogen free (SPF) adult or newborn mice with pet store mice (PSE or BiPSE, respectively). Mice were then exposed to HDM to induce AAD. Results: We found that the effect of increased microbial exposure on the development of allergic airway inflammation differs by age. Increasing exposure to diverse microbes as adults exacerbates the development of allergic airway inflammation, whereas this was not observed when exposure occurred at birth. Conclusion: We suggest that experimental evaluation of the hygiene hypothesis in inflammation, particularly those using mouse models, may need to consider age of the host and time of microbial exposure. Capsule Summary: Mouse models of increased exposure to diverse microbial environment shown to differentially affect the development of allergic airway inflammation, depending on the age of microbial exposure.

  PublisherOA PDFDOI

• Programing Immunogenicity of Dengue EDIII Vaccine Antigens Using Engineered Outer Membrane Vesicles (OMVs)

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-01 · 1 citations

  preprintOpen access

  Abstract Dengue is a mosquito-borne viral infection and is more prevalent in the world with no therapeutics and suboptimal vaccine performance against all four serotypes of the dengue virus. Hence, there is an urgent requirement for a non-infectious and non-replicative vaccine candidate that can elicit a balanced and serotype-specific immune response. In this study, we have engineered bacterial outer membrane vesicles (rOMVs) that display EDIII antigens (EDIII rOMVs). The current formulation modulates the expression of costimulatory molecules on antigen-presenting cells (APCs) as well as enhances the uptake and presentation. Subsequently, the EDIII rOMVs elicited a strong antigen-specific polyfunctional response from CD4+ and CD8+ T cells. The robust antibody response was facilitated by a germinal center reaction characterized by high T follicular helper (Tfh) and B cell response levels in the mice that received EDIII rOMVs. Notably, the produced antibodies demonstrated the ability to neutralize all four dengue virus serotypes in an in vitro infection model, indicating its potential role in protective immunity. Graphical abstract

  PublisherOA PDFDOI

• Abstract P3-01-14: DARC/ACKR1, Duffy-Null and African ancestry influence on immune response in triple negative breast cancer

  Clinical Cancer Research · 2025-06-13

  article

  Abstract Breast cancer (BC) related mortality remains approximately 40% higher among African American women, where women of African ancestry are more frequently diagnosed with the more aggressive molecular subtype of BC, triple negative BC (TNBC). We have previously reported that increased west African ancestry is associated with TNBC diagnoses, and that the African ancestry-specific Duffy-null allele (Fy-) is a risk factor for TNBC diagnoses compared to other BC subtypes. Fy- is an ancestral allele that provides immunity from Plasmodium vivax malaria and is found at frequencies of >90% across Sub-Saharan African populations, and >60% among African Americans. Fy- removes erythrocytic expression of the Duffy Antigen Receptor for Chemokines gene, recently renamed Atypical Chemokine Receptor 1 (DARC/ACKR1). DARC/ACKR1 functions to modulate systemic chemokine levels, and via expression on endothelial cells influences immune cell diapedesis into tissues. In the context of BC, Fy- individuals retain DARC/ACKR1 expression on endothelial cells, and we have recently reported variable DARC/ACKR1 expression on breast tumor epithelial cells using bulk transcriptomics and immunohistochemistry-based methods. Our preliminary work conducted among women of African ancestry suggests that immune cell infiltration is correlated to DARC/ACKR1 epithelial expression. Currently, we aim to describe the combined impact of DARC/ACKR1 on immune response in both the tumor microenvironment and circulation dependent on DARC/ACKR1 expression status. To determine Fy- impact on circulating inflammatory markers of BC patients, we have conducted Luminex multiplex assays to detect and quantify over 40 circulating chemokines and cytokines. Fy- status was determined by WGS of germline, or single-plex PCR genotyping methods. We previously reported univariate associations with CCL2, CXCL2 and CXCL11. In models adjusting for BMI and TNBC status, significant associations with CCL2 and CXCL11 are retained, where we also report significance in univariate and fully adjusted models with CCL1, CCL19, MIF and Resistin. Our ongoing work is evaluating levels associated with Fy- among African Americans only in univariate and adjusted models, and exploring how these profiles may change between molecular subtypes, including TNBC. We have quantified the circulating and tumor immunological/inflammation profiles of (n=100+) TNBC patients using Luminex multiplex assays and tumor-specific transcriptomics. We have discovered associations with (1) Fy- status and chemokine levels in the tumors versus circulation, and (2) differential levels of chemokines in tumors or circulation based on DARC/ACKR1 expression in the breast tumors. To better define these phenotypes spatially, we have utilized imaging mass cytometry to profile breast tumors with varying levels of DARC/ACKR1 expression on the tumor epithelial cells. DARC/ACKR1 positive tumors have increased levels of immune cells infiltrating, with increases in T cell, B cell and macrophage populations. This aligns with our previous reports using bulk transcriptomics data, specifically where we showed an African ancestry associated gene signature enriched in immune response pathways. We are currently working to quantify the spatial resolution of these phenotypes. In conclusion, African ancestry women are more frequently diagnosed with TNBC with aggressive tumor phenotypes that are hard-to-treat. The mechanisms driving this aggressive tumor progression likely involve systemic inflammation. DARC/ACKR1 expression helps regulate systemic inflammatory profiles, which are altered among Fy- patients. We are working to define the impact of these DARC-regulated systemic profiles on the tumor microenvironment among TNBC patients, associated with Fy- DARC status. Specifically, DARC/ACKR1 driven immune profiles may provide new opportunities to for treatment to better serve this population of women. Citation Format: Yanira Guerra, Stevens Patino, Kenya Bynes, Danielle Doucette, Emma Guyonnet, Brian Stonaker, Julie Sahler, Avery August, Jason White, Lisa Newman, Melissa Davis. DARC/ACKR1, Duffy-Null and African ancestry influence on immune response in triple negative breast cancer [abstract]. In: Proceedings of the San Antonio Breast Cancer Symposium 2024; 2024 Dec 10-13; San Antonio, TX. Philadelphia (PA): AACR; Clin Cancer Res 2025;31(12 Suppl):Abstract nr P3-01-14.

  PublisherDOI

• A Randomized Clinical Trial Evaluating Lactiplantibacillus Plantarum for the Prevention of GI aGvHD: A Report From the Children’s Oncology Group (ACCL1633)

  Transplantation and Cellular Therapy · 2025-04-28 · 3 citations

  article
  PublisherDOI

• Replication-incompetent VSV-based vaccine elicits protective responses against SARS-CoV-2 and influenza virus

  Science Advances · 2025-01-29 · 4 citations

  articleOpen access

  Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and influenza viruses lead to severe respiratory illnesses and death in humans, exacerbated in individuals with underlying health conditions, remaining substantial global public health concerns. Here, we developed a bivalent replication-incompetent single-cycle pseudotyped vesicular stomatitis virus vaccine that incorporates both a prefusion-stabilized SARS-CoV-2 spike protein lacking a furin cleavage site and a full-length influenza A virus neuraminidase protein. Vaccination of K18-hACE2 or C57BL/6J mouse models generated durable levels of neutralizing antibodies, T cell responses, and protection from morbidity and mortality upon challenge with either virus. Furthermore, the vaccine provided heterologous protection upon challenge with a different influenza virus strain, supporting the advantage of using NA to increase the breadth of vaccine protection. Now, no bivalent vaccine is approved for use against both SARS-CoV-2 and influenza virus. Our study supports using this platform to develop safe and efficient vaccines against multiple viruses.

  PublisherDOI

• Juneteenth in STEMM and the barriers to equitable science

  UNC Libraries · 2025-03-19

  articleOpen access
  PublisherDOI

• Cell-Free Expression of Nipah Virus Transmembrane Proteins for Proteoliposome Vaccine Design

  ACS Nano · 2025-06-03 · 3 citations

  articleOpen access

  Membrane proteins expressed on the surface of enveloped viruses are potent antigens in a vaccine, yet are difficult to produce and present due to their instability without a lipid scaffold. Current vaccination strategies that incorporate viral membrane proteins, such as live attenuated viruses, inactivated viruses, or extracellular vesicles, have limitations including lengthy production time, poor immunogenicity, extensive processing steps, and/or poor stability. Cell-free protein synthesis of viral membrane proteins offers a rapid, one-step method to assemble vaccine nanoparticles via cotranslational folding of membrane proteins into nanoscale liposomes. Here, we develop a vaccine candidate for the deadly Nipah virus (NiV), a highly lethal virus listed by the World Health Organization as a priority pathogen, by cell-free expressing two full-length Nipah virus membrane proteins. We demonstrate that both NiV fusion protein (NiV F) and NiV glycoprotein (NiV G) can be expressed and cotranslationally integrated into liposomes and that they fold into their native conformation. We find that the removal of a signal peptide sequence and the alteration of liposome lipid composition improve viral membrane protein incorporation. Furthermore, a lipid adjuvant, monophosphoryl lipid A (MPLA), can be readily added to liposomes without disrupting protein-vesicle loading or protein folding conformations. Finally, we demonstrate that our generated liposomal formulations lead to enhanced humoral responses in mice compared to empty and single-protein controls. This work establishes a platform to quickly assemble and present membrane antigens as multivalent vaccines that will enable a rapid response to the broad range of emerging pathogenic threats.

  PublisherOA PDFDOI

Recent grants

• Immuno-Engineering: Integrated Engineering and Immunology Training

  NIH · $756k · 2018–2024

• NIH Grant R01AI073955

  NIH · $1.9M · 2015

• NIH Grant R56AI073955

  NIH · $61k · 2008

• Selective Aryl Hydrocarbon Receptor Modulators and T cell Effector Function

  NIH · $430k · 2014–2017

• A novel murine model of allergic airway inflammation.

  NIH · $443k · 2018–2022

Frequent coauthors

• Weishan Huang

  Louisiana State University

  109 shared

• Weishan Huang

  University of Chinese Academy of Sciences

  41 shared

• Bo Dupont

  35 shared

• Julie Sahler

  Cornell University

  33 shared

• Brian Imbiakha

  Cornell University

  29 shared

• Hidesaburô Hanafusa

  28 shared

• David W. Buchholz

  New York State College of Veterinary Medicine

  28 shared

• Hector C. Aguilar

  Cornell University

  23 shared

Labs

• AUGUST LABPI

  CURRENT AUGUST LAB MEMBERS

Awards & honors

• HHMI Professor
• Deputy Provost