Slim Fourati

Assistant Professor

Northwestern University Feinberg School of Medicine

United States

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Dr. Slim Fourati is an Assistant Professor at Northwestern University Feinberg School of Medicine in the United States. His research areas include immunology, vaccine response, and the immune correlates of infectious diseases such as HIV and COVID-19. Recent publications highlight the impact of pre-existing infections on vaccine efficacy and the predictive models of antibody responses to various vaccines.

Articles (10)

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2023

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2023

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2023

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2022

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2022

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2022

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2021

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2021

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2021

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2020

Collaborators (6)

Suzanna Chak

University of California, San Francisco

UNITED STATES

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Lewis Tomalin

Icahn School of Medicine at Mount Sinai

UNITED STATES

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Namal Liyanage

Assistant Professor

The Ohio State University Wexner Medical Center

UNITED STATES

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Joann Diray Arce

Assistant Professor

Boston Children's Hospital

UNITED STATES

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Michael Wilson

Professor

University of California, San Francisco

UNITED STATES

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Cole Maguire

University of Texas at Austin

UNITED STATES

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Slim Fourati

Research Interests

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Articles (10)

Multi-omic longitudinal study reveals immune correlates of clinical course among hospitalized COVID-19 patients.

Schistosoma mansoni infection alters the host pre-vaccination environment resulting in blunted Hepatitis B vaccination immune responses.

HIV vaccine candidate efficacy in female macaques mediated by cAMP-dependent efferocytosis and V2-specific ADCC

Pan-vaccine analysis reveals innate immune endotypes predictive of antibody responses to vaccination

Transcriptional atlas of the human immune response to 13 vaccines reveals a common predictor of vaccine-induced antibody responses

The Immune Signatures data resource, a compendium of systems vaccinology datasets

The transcription factor CREB1 is a mechanistic driver of immunogenicity and reduced HIV-1 acquisition following ALVAC vaccination

Single cell RNA sequencing of AML initiating cells reveals RNA-based evolution during disease progression

Monocyte-derived transcriptome signature indicates antibody-dependent cellular phagocytosis as a potential mechanism of vaccine-induced protection against HIV-1

Engagement of monocytes, NK cells, and CD4+ Th1 cells by ALVAC-SIV vaccination results in a decreased risk of SIVmac251 vaginal acquisition.

Collaborators (6)

Suzanna Chak

Lewis Tomalin

Namal Liyanage

Joann Diray Arce

Michael Wilson

Cole Maguire

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