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Home / Equine Research Bank / Infect Immun / Rhodococcus equi-infected macrophages are recognized and kil...
Infection and immunity2004; 72(12); 7073-7083; doi: 10.1128/IAI.72.12.7073-7083.2004

Rhodococcus equi-infected macrophages are recognized and killed by CD8+ T lymphocytes in a major histocompatibility complex class I-unrestricted fashion.

Abstract: The goal of this research was to examine the role of cytotoxic T lymphocytes (CTL) in the control of Rhodococcus equi and specifically to determine if R. equi-specific CD8+ CTL occurred in the blood of immune horses. Equine peripheral blood mononuclear cells stimulated with antigen-presenting cells either infected with R. equi or exposed to soluble R. equi antigen lysed R. equi-infected target cells. Lysis was decreased to background by depletion of either CD2+ or CD3+ cells, indicating that the effector cell had a T-lymphocyte, but not NK cell, phenotype. Stimulation induced an increased percentage of CD8+ T cells in the effector population, and depletion of CD8+ T cells resulted in significantly decreased lysis of infected targets. Killing of R. equi-infected macrophages by effector cells was equally effective against autologous and equine leukocyte antigen A (classical major histocompatibility complex [MHC] class I) mismatched targets. To evaluate potential target antigens, target cells were infected with either virulent (80.6-kb plasmid-containing) or avirulent (plasmid-cured) R. equi. The degree of lysis was not altered by the presence of the plasmid, providing evidence that the virulence plasmid, which is required for survival within macrophages, was not necessary for recognition and killing of R. equi-infected cells. These data indicate that immunocompetent adult horses develop R. equi-specific CD8+ CTL, which may play a role in immunity to R. equi. The apparent lack of restriction via classical MHC class I molecules suggests a novel or nonclassical method of antigen processing and presentation, such as presentation by CD1 or other nonclassical MHC molecules.
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Publication Date: 2004-11-24 PubMed ID: 15557631PubMed Central: PMC529141DOI: 10.1128/IAI.72.12.7073-7083.2004Google Scholar: Lookup
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  • Non-U.S. Gov't
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  • U.S. Gov't
  • P.H.S.

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research investigates the role of T lymphocytes in controlling the bacterium Rhodococcus equi in horses. The results led the researchers to suggest that these immune cells can recognize and destroy this bacterium in a fashion that goes beyond the typically understood immune processes.

Research Objectives and Methods

  • The scientists set out to examine the role cytotoxic T lymphocytes (CTLs) play in controlling Rhodococcus equi, a bacterium that primarily affects the lungs of foals but can also cause infections in humans.
  • Specifically, they wanted to understand if there were R. equi-specific CD8+ CTLs in the blood of immune horses.
  • Equine peripheral blood mononuclear cells were stimulated with antigen-presenting cells that were either infected with R. equi or exposed to a soluble form of the bacteria.

Key Findings

  • The researchers found that the stimulated immune cells generated cytotoxic T lymphocytes that killed R. equi-infected target cells, suggesting that the CTLs recognized and responded to the R. equi bacteria.
  • These effects disappeared when CD2+ or CD3+ cells were removed, indicating that the effector cell killing R. equi has a T-lymphocyte phenotype, meaning it’s a type of T cell rather than a natural killer (NK) cell.
  • The stimulating process prompted an increase in the percentage of CD8+ T cells, and the removal of these cells significantly reduced the death of infected targets, providing further evidence of their crucial role.
  • The T cells were found to kill the R. equi bacteria regardless of whether the bacteria were “autologous” (self) or “mismatched” (foreign). This suggests that there might be a different or nonclassical method of antigen processing and presentation going on.
  • Further, when the target cells were infected with either virulent or nonvirulent strains of R. equi, the percentage of killed cells remained unchanged, which indicates that the presence of the virulence plasmid (a piece of bacterial DNA critical for the bacteria’s survival) is not necessary for the CTL’s recognition and destruction of R. equi.

Implicatioms of the Study

  • These results imply that immune competent adult horses can develop R. equi-specific CD8+ CTLs, which may contribute to immunity against R. equi.
  • The findings suggest that a unique process may be involved in how these immune cells process and present antigens, a revelation that could be harnessed to develop new therapeutic strategies against R. equi infections in horses and potentially in humans.

Cite This Article

APA
Patton KM, McGuire TC, Fraser DG, Hines SA. (2004). Rhodococcus equi-infected macrophages are recognized and killed by CD8+ T lymphocytes in a major histocompatibility complex class I-unrestricted fashion. Infect Immun, 72(12), 7073-7083. https://doi.org/10.1128/IAI.72.12.7073-7083.2004

Publication

Infection and immunity
ISSN: 0019-9567
NlmUniqueID: 0246127
Country: United States
Language: English
Volume: 72
Issue: 12
Pages: 7073-7083

Researcher Affiliations

Patton, Kristin M
  • Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, WA 99164-7040, USA
McGuire, Travis C
    Fraser, Darrilyn G
      Hines, Stephen A

        MeSH Terms

        • Animals
        • Antigen Presentation
        • CD2 Antigens / analysis
        • CD3 Complex / analysis
        • CD8-Positive T-Lymphocytes / immunology
        • Cytotoxicity, Immunologic
        • Histocompatibility Antigens Class I / physiology
        • Horses
        • Macrophages / microbiology
        • Rhodococcus equi / genetics
        • Rhodococcus equi / immunology
        • Rhodococcus equi / pathogenicity
        • Virulence

        Grant Funding

        • 5K08 AI 049391-03 / NIAID NIH HHS

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