Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Mycobacterium tuberculosis regulates CD1 antigen presentation pathways through TLR-2.

Carme Roura-Mir1, Lisheng Wang, Tan-Yun Cheng

  • 1Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|July 22, 2005
PubMed
Summary

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Conserved T cell receptor usage underpins recognition of CD1c presenting a mycobacterial lipid.

bioRxiv : the preprint server for biology·2026
Same author

CD1a-Mediated Presentation of Canonical Microbial Peptides to T Cells.

bioRxiv : the preprint server for biology·2026
Same author

HLA-DRB1 Allelic Combinations Differentially Shape Dendritic Cell Antigen Presentation Enhanced by Tumour Cell Line Lysate-Pulsing.

HLA·2026
Same author

Protein kinase F regulates the virulence of <i>Mycobacterium tuberculosis</i>.

bioRxiv : the preprint server for biology·2026
Same author

Sideways lipid presentation by the antigen-presenting molecule CD1c.

Nature communications·2025
Same author

Emerging Roles of CD1 and Lipids in Human Health and Disease.

Annual review of immunology·2025

Mycobacterium tuberculosis infection induces myeloid cells to present lipid antigens via group 1 CD1 proteins. Mycobacterial lipids activate T cells and antigen-presenting cells through Toll-like receptor 2 (TLR-2).

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Mycobacterium tuberculosis (M. tuberculosis) is a significant global pathogen.
  • Lipid antigens from M. tuberculosis are presented to human T cells during infection.

Purpose of the Study:

  • To investigate how M. tuberculosis infection influences antigen-presenting cells (APCs).
  • To identify the mechanisms by which mycobacterial components activate T cell responses.

Main Methods:

  • Infection of myeloid precursors with live M. tuberculosis or exposure to cell wall products.
  • Analysis of CD1 protein expression using transcriptional and protein synthesis studies.
  • Isolation and identification of CD1-inducing factors using chromatography and chemical synthesis.
  • Assessment of Toll-like receptor 2 (TLR-2) involvement in CD1 upregulation.

Related Experiment Videos

Main Results:

  • Cellular infection or exposure to mycobacterial products converted CD1- myeloid precursors into APCs expressing group 1 CD1 proteins (CD1a, CD1b, CD1c).
  • Upregulation of group 1 CD1 proteins occurred via transcriptional regulation and new protein synthesis, with concurrent downregulation of CD1d.
  • Polar lipids from M. tuberculosis signaled through TLR-2, which was essential for CD1 protein expression.
  • Mycobacterial cell wall lipids provide dual signals: lipid antigens for T cell receptor activation and lipid adjuvants for TLR-2-mediated APC activation.

Conclusions:

  • Mycobacterial lipids act as potent immune modulators, influencing both antigen presentation and APC activation.
  • The dual signaling mechanism may selectively enhance the presentation of foreign lipids by APCs encountering M. tuberculosis.
  • This study elucidates a novel pathway for T cell activation in tuberculosis, highlighting the role of lipid antigens and TLR-2 signaling.