Lin‐Xi Li
Associate Professor
faculty
Microbiology & Immunology, College of Medicine
Research Areas
Biography and Research Information
OverviewAI-generated summary
Lin-Xi Li's research focuses on understanding the mechanisms of immune responses to infectious agents, particularly Chlamydia, and their impact on host health. Her work has explored the role of specific immune cells and signaling pathways in controlling Chlamydia dissemination and establishing protective immunity in the female reproductive tract. This includes investigating the differentiation and function of CD4 T cells, as well as the interplay between T cells and other immune components like antibodies.
Beyond Chlamydia, Li's research extends to other microbial infections, such as Mycobacterium tuberculosis, examining the role of immune cells like neutrophils and macrophages in conferring protection. She also investigates host immune responses in the context of disease models, including studies on hypertension, exploring the involvement of immune pathways and cellular interactions in its development and regulation. Her federally funded research, totaling over $558,000 from NIH/NIAID, supports her investigations into early protective immune responses and the mechanisms of memory CD4 T cell-mediated immunity against Chlamydia.
Li holds an h-index of 13 with 33 publications and 696 citations. She collaborates extensively with researchers at the University of Arkansas for Medical Sciences, including Miguel A. B. Mercado, J. Tucker Andrews, Lu Huang, and Rachel S. Palmer, with whom she has co-authored multiple publications.
Metrics
- h-index: 13
- Publications: 33
- Citations: 704
Selected Publications
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β-glucan-induced monocyte-derived alveolar macrophages confer protection against Mycobacterium tuberculosis 4395 (2025)
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The roles of TGFb signaling in CD4 T cell responses to Chlamydia infection in the female reproductive tract 9284 (2025)
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CXCR6+ polyfunctional CD4 T cells are essential for protective immunity against Chlamydia in the female reproductive tract (2024)
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Metabolically active neutrophils represent a permissive niche for Mycobacterium tuberculosis (2024)
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BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against Chlamydia (2024)
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BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against <i>Chlamydia</i> (2023)
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Transcription factor Bhlhe40 plays a protective role during intravaginal <i>Chlamydia muridarum</i> infection in mice (2023)
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Metabolism and ontogeny of alveolar macrophages contribute to peripheral trained immunity and confer protection against <i>Mycobacterium tuberculosis</i> (2023)
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IFNγ and Antibody Synergize To Enhance Protective Immunity against Chlamydia Dissemination and Female Reproductive Tract Reinfections (2022)
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IFNγ and antibody synergize to enhance protective immunity against <i>Chlamydia</i> dissemination and female reproductive tract reinfections (2022)
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Breast adipose regulation of premenopausal breast epithelial phenotype involves interleukin 10 (2021)
Federal Grants 2 $558,240 total
Mechanisms of memory CD4 T cell-mediated immune protection against Chlamydia
Grants & Funding
- T cell homing to the kidney contributes to salt retention and blood pressure regulation - Continuation NIH/Nat. Heart, Lung & Blood Institute Co-Investigator
- Mechanisms of memory CD4 T cell-mediated immune protection against Chlamydia - Continuation NIH/Nat. Inst. of Allergy & Infectious Diseases Principal Investigator
- Exploring early protective immune responses to Chlamydia NIH/Nat. Inst. of Allergy & Infectious Diseases Principal Investigator
- Exploring early protective immune responses to Chlamydia NIH/Nat. Inst. of Allergy & Infectious Diseases Principal Investigator
- Exploring early protective immune responses to Chlamydia NIH/Nat. Inst. of Allergy & Infectious Diseases Principal Investigator
- Exploring early protective immune responses to Chlamydia NIH/Nat. Inst. of Allergy & Infectious Diseases Principal Investigator
Collaboration Network
Top Collaborators
- The IFNγ-PDL1 Pathway Enhances CD8T-DCT Interaction to Promote Hypertension
- Metabolically active neutrophils represent a permissive niche for Mycobacterium tuberculosis
- <i>P2X7</i> -Mediated Antigen-Independent Activation of CD8 <sup>+</sup> T Cells Promotes Salt-Sensitive Hypertension
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against Chlamydia
- Metabolism and ontogeny of alveolar macrophages contribute to peripheral trained immunity and confer protection against <i>Mycobacterium tuberculosis</i>
Showing 5 of 8 shared publications
- IFNγ and Antibody Synergize To Enhance Protective Immunity against Chlamydia Dissemination and Female Reproductive Tract Reinfections
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against Chlamydia
- IFNγ and antibody synergize to enhance protective immunity against <i>Chlamydia</i> dissemination and female reproductive tract reinfections
- Transcription factor Bhlhe40 plays a protective role during intravaginal <i>Chlamydia muridarum</i> infection in mice
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against <i>Chlamydia</i>
Showing 5 of 6 shared publications
- The IFNγ-PDL1 Pathway Enhances CD8T-DCT Interaction to Promote Hypertension
- Metabolically active neutrophils represent a permissive niche for Mycobacterium tuberculosis
- <i>P2X7</i> -Mediated Antigen-Independent Activation of CD8 <sup>+</sup> T Cells Promotes Salt-Sensitive Hypertension
- Metabolism and ontogeny of alveolar macrophages contribute to peripheral trained immunity and confer protection against <i>Mycobacterium tuberculosis</i>
- β-glucan-induced monocyte-derived alveolar macrophages confer protection against Mycobacterium tuberculosis 4395
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against Chlamydia
- Transcription factor Bhlhe40 plays a protective role during intravaginal <i>Chlamydia muridarum</i> infection in mice
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against <i>Chlamydia</i>
- CXCR6+ polyfunctional CD4 T cells are essential for protective immunity against Chlamydia in the female reproductive tract
- The roles of TGFb signaling in CD4 T cell responses to Chlamydia infection in the female reproductive tract 9284
- The IFNγ-PDL1 Pathway Enhances CD8T-DCT Interaction to Promote Hypertension
- Metabolically active neutrophils represent a permissive niche for Mycobacterium tuberculosis
- <i>P2X7</i> -Mediated Antigen-Independent Activation of CD8 <sup>+</sup> T Cells Promotes Salt-Sensitive Hypertension
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against Chlamydia
- Transcription factor Bhlhe40 plays a protective role during intravaginal <i>Chlamydia muridarum</i> infection in mice
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against <i>Chlamydia</i>
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against Chlamydia
- Transcription factor Bhlhe40 plays a protective role during intravaginal <i>Chlamydia muridarum</i> infection in mice
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against <i>Chlamydia</i>
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against Chlamydia
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against <i>Chlamydia</i>
- CXCR6+ polyfunctional CD4 T cells are essential for protective immunity against Chlamydia in the female reproductive tract
- The IFNγ-PDL1 Pathway Enhances CD8T-DCT Interaction to Promote Hypertension
- <i>P2X7</i> -Mediated Antigen-Independent Activation of CD8 <sup>+</sup> T Cells Promotes Salt-Sensitive Hypertension
- The IFNγ-PDL1 Pathway Enhances CD8T-DCT Interaction to Promote Hypertension
- <i>P2X7</i> -Mediated Antigen-Independent Activation of CD8 <sup>+</sup> T Cells Promotes Salt-Sensitive Hypertension
- The IFNγ-PDL1 Pathway Enhances CD8T-DCT Interaction to Promote Hypertension
- <i>P2X7</i> -Mediated Antigen-Independent Activation of CD8 <sup>+</sup> T Cells Promotes Salt-Sensitive Hypertension
- The IFNγ-PDL1 Pathway Enhances CD8T-DCT Interaction to Promote Hypertension
- <i>P2X7</i> -Mediated Antigen-Independent Activation of CD8 <sup>+</sup> T Cells Promotes Salt-Sensitive Hypertension
- The IFNγ-PDL1 Pathway Enhances CD8T-DCT Interaction to Promote Hypertension
- <i>P2X7</i> -Mediated Antigen-Independent Activation of CD8 <sup>+</sup> T Cells Promotes Salt-Sensitive Hypertension
- The IFNγ-PDL1 Pathway Enhances CD8T-DCT Interaction to Promote Hypertension
- <i>P2X7</i> -Mediated Antigen-Independent Activation of CD8 <sup>+</sup> T Cells Promotes Salt-Sensitive Hypertension
- IFNγ and Antibody Synergize To Enhance Protective Immunity against Chlamydia Dissemination and Female Reproductive Tract Reinfections
- IFNγ and antibody synergize to enhance protective immunity against <i>Chlamydia</i> dissemination and female reproductive tract reinfections
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