Miguel A. B. Mercado

Researcher

UAMS

Faculty Researcher

4 h-index 10 pubs 42 cited

Research Areas

Biomedical Subjects

Links

Research Group

OverviewAI-generated summary

Miguel A. B. Mercado's research focuses on understanding the immune responses to Chlamydia infections, particularly within the female reproductive tract. His work investigates the roles of specific immune cells and transcription factors in mediating protective immunity and the potential for reinfection. Recent publications by Mercado and collaborators explore how IFNγ and antibodies synergize to enhance immunity against Chlamydia dissemination and reinfections. Further research examines the function of the transcription factor BHLHE40 in driving CD4 T cell differentiation and its protective role during intravaginal Chlamydia muridarum infection in mice. Additionally, his work has delved into the influence of TGFb signaling on CD4 T cell responses to Chlamydia in the female reproductive tract. Mercado's scholarship metrics include an h-index of 3, with 10 total publications and 41 citations. He has collaborated with researchers such as Lin‐Xi Li, Yejin Kim, and Rachel S. Palmer, all from the University of Arkansas for Medical Sciences.

Metrics

h-index: 4
Publications: 10
Citations: 42

Selected Publications

CXCR6 marks polyfunctional effector CD4 T cells required for anti- Chlamydia immunity in the female reproductive tract (2026)

bioRxiv (Cold Spring Harbor Laboratory) DOI OpenAlex
The roles of TGFb signaling in CD4 T cell responses to Chlamydia infection in the female reproductive tract 9284 (2025)

The Journal of Immunology DOI OpenAlex
BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against Chlamydia (2024)

PLoS Pathogens 4 citations DOI OpenAlex
BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against Chlamydia (2023)

bioRxiv (Cold Spring Harbor Laboratory) DOI OpenAlex
Transcription factor Bhlhe40 plays a protective role during intravaginal Chlamydia muridarum infection in mice (2023)

The Journal of Immunology DOI OpenAlex
IFNγ and Antibody Synergize To Enhance Protective Immunity against Chlamydia Dissemination and Female Reproductive Tract Reinfections (2022)

Infection and Immunity 4 citations DOI OpenAlex
IFNγ and antibody synergize to enhance protective immunity against Chlamydia dissemination and female reproductive tract reinfections (2022)

bioRxiv (Cold Spring Harbor Laboratory) DOI OpenAlex
Innate IFN-γ Is Essential for Systemic Chlamydia muridarum Control in Mice, While CD4 T Cell-Dependent IFN-γ Production Is Highly Redundant in the Female Reproductive Tract (2020)

Infection and Immunity 21 citations DOI OpenAlex
Innate IFNγ is essential for systemic Chlamydia control while CD4 T cell-dependent IFNγ production is highly redundant in the female reproductive tract (2020)

bioRxiv (Cold Spring Harbor Laboratory) 1 citation DOI OpenAlex
Antibody, but not B‐cell–dependent antigen presentation, plays an essential role in preventing Chlamydia systemic dissemination in mice (2020)

European Journal of Immunology 12 citations DOI OpenAlex