Publication

CD4 T Cells in Mycobacterium tuberculosis and Schistosoma mansoni Co-infected Individuals Maintain Functional TH1 Responses

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Last modified
  • 05/14/2025
Type of Material
Authors
    Taryn A. McLaughlin, Emory UniversityJeremiah Khayumbi, Kenya Medical Research InstituteJoshua Ongalo, Kenya Medical Research InstituteJoan Tonui, Kenya Medical Research InstituteAngela Campbell, Emory UniversitySalim Allana, Emory UniversitySamuel Gurrion Ouma, Kenya Medical Research InstituteFelix Hayara Odhiambo, Kenya Medical Research InstituteNeel Gandhi, Emory UniversityCheryl Day, Emory University
Language
  • English
Date
  • 2020-02-07
Publisher
  • Frontiers Media
Publication Version
Copyright Statement
  • © Copyright © 2020 McLaughlin, Khayumbi, Ongalo, Tonui, Campbell, Allana, Gurrion Ouma, Odhiambo, Gandhi and Day.
License
Final Published Version (URL)
Title of Journal or Parent Work
ISSN
  • 1664-3224
Volume
  • 11
Start Page
  • 127
End Page
  • 127
Grant/Funding Information
  • This study was supported by grants to CD from the National Institute of Allergy and Infectious Diseases at the National Institutes of Health (5R01AI111948 and U19AI111211).
  • NG was supported by grants from the National Institute of Allergy and Infectious Diseases at the National Institutes of Health (K24AI114444, U19AI111211).
Supplemental Material (URL)
Abstract
  • Mycobacterium tuberculosis (Mtb) is a serious public health concern, infecting a quarter of the world and leading to 10 million cases of tuberculosis (TB) disease and 1. 5 million deaths annually. An effective type 1 CD4 T cell (TH1) immune response is necessary to control Mtb infection and defining factors that modulate Mtb-specific TH1 immunity is important to better define immune correlates of protection in Mtb infection. Helminths stimulate type 2 (TH2) immune responses, which antagonize TH1 cells. As such, we sought to evaluate whether co-infection with the parasitic helminth Schistosoma mansoni (SM) modifies CD4 T cell lineage profiles in a cohort of HIV-uninfected adults in Kisumu, Kenya. Individuals were categorized into six groups by Mtb and SM infection status: healthy controls (HC), latent Mtb infection (LTBI) and active tuberculosis (TB), with or without concomitant SM infection. We utilized flow cytometry to evaluate the TH1/TH2 functional and phenotypic lineage state of total CD4 T cells, as well as CD4 T cells specific for the Mtb antigens CFP-10 and ESAT-6. Total CD4 T cell lineage profiles were similar between SM+ and SM− individuals in all Mtb infection groups. Furthermore, in both LTBI and TB groups, SM infection did not impair Mtb-specific TH1 cytokine production. In fact, SM+ LTBI individuals had higher frequencies of IFNγ+ Mtb-specific CD4 T cells than SM− LTBI individuals. Mtb-specific CD4 T cells were characterized by expression of both classical TH1 markers, CXCR3 and T-bet, and TH2 markers, CCR4, and GATA3. The expression of these markers was similar between SM+ and SM− individuals with LTBI. However, SM+ individuals with active TB had significantly higher frequencies of GATA3+ CCR4+ TH1 cytokine+ Mtb-specific CD4 T cells, compared with SM− TB individuals. Together, these data indicate that Mtb-specific TH1 cytokine production capacity is maintained in SM-infected individuals, and that Mtb-specific TH1 cytokine+ CD4 T cells can express both TH1 and TH2 markers. In high pathogen burden settings where co-infection is common and reoccurring, plasticity of antigen-specific CD4 T cell responses may be important in preserving Mtb-specific TH1 responses.
Author Notes
Keywords
Research Categories
  • Biology, Microbiology
  • Health Sciences, Immunology

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