Miguel A. B. Mercado

Researcher

Last publication 2025 Last refreshed 2026-05-16

faculty

3 h-index 10 pubs 41 cited

Biography and Research Information

OverviewAI-generated summary

Miguel A. B. Mercado's research focuses on the immune response to Chlamydia infections, particularly in the female reproductive tract. His work investigates the role of specific immune cells and molecular factors in conferring protection against Chlamydia dissemination and reinfection. Recent publications by Mercado and his collaborators explore the synergistic effects of interferon-gamma (IFNγ) and antibodies in enhancing protective immunity. Additionally, his research examines the function of the transcription factor BHLHE40 in driving protective CD4 T cell differentiation and its role in the host's defense against Chlamydia muridarum infection in mouse models. Mercado also studies the influence of TGF-beta signaling pathways on CD4 T cell responses within the context of Chlamydia infection in the female reproductive tract.

Metrics

  • h-index: 3
  • Publications: 10
  • Citations: 41

Selected Publications

  • The roles of TGFb signaling in CD4 T cell responses to Chlamydia infection in the female reproductive tract 9284 (2025)
  • BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against Chlamydia (2024)
    2 citations DOI OpenAlex
  • BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against <i>Chlamydia</i> (2023)
  • Transcription factor Bhlhe40 plays a protective role during intravaginal <i>Chlamydia muridarum</i> infection in mice (2023)
  • IFNγ and Antibody Synergize To Enhance Protective Immunity against Chlamydia Dissemination and Female Reproductive Tract Reinfections (2022)
    4 citations DOI OpenAlex
  • IFNγ and antibody synergize to enhance protective immunity against <i>Chlamydia</i> dissemination and female reproductive tract reinfections (2022)

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Collaboration Network

11 Collaborators 1 Institution 1 Country

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