Jason A. Hall

National Institute of Allergy and Infectious Diseases

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Yasmine Belkaid

National Institute of Allergy and Infectious Diseases

Dan R. Littman

New York University

June‐Yong Lee

Yonsei University

Nicolas Bouladoux

National Institutes of Health

John R. Grainger

Manchester Academic Health Science Centre

Lin Wu

New York University

Maria Pokrovskii

New York University

Lina Kroehling

Boston University

Guillaume Oldenhove

Université Libre de Bruxelles

Emily R. Miraldi

Cincinnati Children's Hospital Medical Center

Cooperative Institutions

National Institutes of Health

National Institute of Allergy and Infectious Diseases

New York University

National Cancer Institute

Center for Cancer Research

Harvard University

University of Chicago

Howard Hughes Medical Institute

University of Pennsylvania

National Heart Lung and Blood Institute

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Combination of Ibrutinib with CD19 Chimeric Antigen Receptor (CAR) T Cells Suggests Greater Contribution to CAR T-Cell Efficacy Than Other Approved BTK Inhibitors in the Preclinical Setting

Blood (2023)

Vicki Plaks Vidusha Cyril Peter A. Riedell Qianqian Zhao Jason A. Hall

10.1182/blood-2023-181805

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Rorα Enforces Stability of the T-Helper-17 Cell Effector Program

SSRN Electronic Journal (2020)

June‐Yong Lee Jason A. Hall Maria Pokrovskii Lina Kroehling Lin Wu

T helper 17 (Th17) cells regulate mucosal barrier defenses, but also promote multiple autoinflammatory diseases. Although many molecular determinants of Th17 cell differentiation have been described, the transcriptional programs that sustain Th17 cells in vivo remain obscure. The transcription factor RORγt is critical for Th17 cell differentiation, but a distinct role of the closely-related RORα, which is co-expressed in Th17 cells, is not known. Here we demonstrate that, although dispensable for Th17 cell differentiation, RORα governs optimal Th17 responses in peripheral tissues. Thus, the absence of RORα in T cells led to significant reductions in both RORγt expression and effector function amongst Th17 cells, due to need for cooperative RORα and RORγt binding to a newly-identified Rorc enhancer element that is essential for Th17 lineage maintenance in vivo. Altogether, these data point to a nonredundant role of RORα in Th17 lineage maintenance via reinforcement of the RORγt transcriptional program.

10.2139/ssrn.3758209

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Citations (1)

Small intestine lamina propria dendritic cells promote de novo generation of Foxp3 T reg cells via retinoic acid

The Journal of Experimental Medicine (2007)

Cheng‐Ming Sun Jason A. Hall Rebecca B. Blank Nicolas Bouladoux Mohamed Oukka

To maintain immune homeostasis, the intestinal immune system has evolved redundant regulatory strategies. In this regard, the gut is home to a large number of regulatory T (T reg) cells, including the Foxp3+ T reg cell. Therefore, we hypothesized that the gut environment preferentially supports extrathymic T reg cell development. We show that peripheral conversion of CD4+ T cells to T reg cells occurs primarily in gut-associated lymphoid tissue (GALT) after oral exposure to antigen and in a lymphopenic environment. Dendritic cells (DCs) purified from the lamina propria (Lp; LpDCs) of the small intestine were found to promote a high level of T reg cell conversion relative to lymphoid organ–derived DCs. This enhanced conversion by LpDCs was dependent on TGF-β and retinoic acid (RA), which is a vitamin A metabolite highly expressed in GALT. Together, these data demonstrate that the intestinal immune system has evolved a self-contained strategy to promote T reg cell neoconversion.

Lamina propria

Gut-associated lymphoid tissue

Microfold cell

10.1084/jem.20070602

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Citations (1,820)

Retinoic Acid Enhances Foxp3 Induction Indirectly by Relieving Inhibition from CD4+CD44hi Cells

Immunity (2008)

Jonathan A. Hill Jason A. Hall Cheng‐Ming Sun Qi Cai Norbert B. Ghyselinck

BETA (programming language)

10.1016/j.immuni.2008.09.018

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Citations (350)

Vitamin A derived retinoic acid signaling mediates intestinal immune homeostasis and immunity

Cytokine (2009)

Jason A. Hall Chengming Sun Guillaume Oldenhove Elizabeth A. Wohlfert Robin Kastenmeyer

Crosstalk

10.1016/j.cyto.2009.07.359

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Citations (1)

RORα enforces stability of the T-helper-17 cell effector program

bioRxiv (Cold Spring Harbor Laboratory) (2020)

June‐Yong Lee Jason A. Hall Maria Pokrovskii Lina Kroehling Lin Wu

Summary T helper 17 (Th17) cells regulate mucosal barrier defenses, but also promote multiple autoinflammatory diseases. Although many molecular determinants of Th17 cell differentiation have been described, the transcriptional programs that sustain Th17 cells in vivo remain obscure. The transcription factor RORγt is critical for Th17 cell differentiation, but a distinct role of the closely-related RORα, which is co-expressed in Th17 cells, is not known. Here we demonstrate that, although dispensable for Th17 cell differentiation, RORα governs optimal Th17 responses in peripheral tissues. Thus, the absence of RORα in T cells led to significant reductions in both RORγt expression and effector function amongst Th17 cells, due to need for cooperative RORα and RORγt binding to a newly-identified Rorc enhancer element that is essential for Th17 lineage maintenance in vivo . Altogether, these data point to a non-redundant role of RORα in Th17 lineage maintenance via reinforcement of the RORγt transcriptional program.

Lineage (genetic)

10.1101/2020.12.15.422921

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Citations (1)

Response to Letter from Mucida et al.

Immunity (2009)

Jonathan A. Hill Jason A. Hall Chengming Sun Qi Cai Norbert B. Ghyselinck

10.1016/j.immuni.2009.03.012

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Citations (6)

Serum Amyloid A Proteins Induce Pathogenic Th17 Cells and Promote Inflammatory Disease

Cell (2019)

June‐Yong Lee Jason A. Hall Lina Kroehling Lin Wu Tariq Ahmad Najar

Innate lymphoid cell

10.1016/j.cell.2019.11.026

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Citations (335)

Serum Amyloid a Proteins Induce Pathogenic T <sub>H</sub>17 Cells and Promote Inflammatory Disease

SSRN Electronic Journal (2019)

June‐Yong Lee Jason A. Hall Lina Kroehling Lin Wu Tariq Ahmad Najar

Lymphoid cells that produce IL-17 cytokines protect barrier tissues from pathogenic microbes, but are also prominent effectors of inflammation and autoimmune disease. T-helper (TH17) cells, defined by RORγt-dependent production of IL-17A and IL-17F, exert homeostatic functions in the gut upon microbiota-directed differentiation from naïve CD4+ T cells. In the non-pathogenic setting, their cytokine production is regulated by serum amyloid A proteins (SAA1 and SAA2) secreted by adjacent intestinal epithelial cells. However, TH17 cell behaviors vary markedly according to their environment. Here we show that SAAs additionally direct a pathogenic pro-inflammatory TH17 cell differentiation program, acting directly on T cells in collaboration with STAT3-activating cytokines. Using loss- and gain-of-function mouse models, we show that SAA1, SAA2, and SAA3 have distinct systemic and local functions in promoting TH17-mediated inflammatory diseases. These studies suggest that T cell signaling pathways modulated by the SAAs may be attractive targets for anti-inflammatory therapies.

Amyloid (mycology)

10.2139/ssrn.3411254

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Commensal DNA Limits Regulatory T Cell Conversion and Is a Natural Adjuvant of Intestinal Immune Responses

Immunity (2008)

Jason A. Hall Nicolas Bouladoux Cheng‐Ming Sun Elizabeth A. Wohlfert Rebecca B. Blank

10.1016/j.immuni.2008.08.009

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Citations (488)