TB Research

<i>Mycobacterium tuberculosis</i> H37Rv Strain Increases the Frequency of CD3<sup>+</sup>TCR<sup>+</sup> Macrophages and Affects Their Phenotype, but Not Their Migration Ability

Ramon-Luing LA, Carranza C, Téllez-Navarrete NA, Medina-Quero K, Gonzalez Y, Torres M, Chavez-Galan L

International journal of molecular sciences · 2021-12

Abstract

In mycobacterial infections, the number of cells from two newly discovered subpopulations of CD3 + myeloid cells are increased at the infection site; one type expresses the T cell receptor (CD3 + TCRαβ + ) and the other does not (CD3 + TCRαβ - ). The role of Mycobacterium tuberculosis (Mtb) virulence in generating these subpopulations and the ability of these cells to migrate remains unclear. In this study, monocyte-derived macrophages (MDMs) infected in vitro with either a virulent (H37Rv) or an avirulent (H37Ra) Mtb strain were phenotypically characterized based on three MDM phenotypes (CD3 - , CD3 + TCRαβ + , and CD3 + TCRαβ - ); then, their migration ability upon Mtb infection was evaluated. We found no differences in the frequency of CD3 + MDMs at 24 h of infection with either Mtb strain. However, H37Rv infection increased the frequency of CD3 + TCRαβ + MDMs at a multiplicity of infection of 1 and altered the expression of CD1b, CD1c, and TNF on the surface of cells from both the CD3 + MDM subpopulations; it also modified the expression of CCR2, CXCR1, and CCR7, thus affecting CCL2 and IL-8 levels. Moreover, H37Rv infection decreased the migration ability of the CD3 - MDMs, but not CD3 + MDMs. These results confirm that the CD3 + macrophage subpopulations express chemokine receptors that respond to chemoattractants, facilitating cell migration. Together, these data suggest that CD3 + MDMs are a functional subpopulation involved in the immune response against Mtb.

MeSH terms

  • Monocytes
  • Macrophages
  • Humans
  • Mycobacterium tuberculosis
  • Tuberculosis
  • Inflammation
  • Tumor Necrosis Factor-alpha
  • Receptors, Chemokine
  • Receptors, Antigen, T-Cell
  • Receptors, Tumor Necrosis Factor
  • Ligands
  • Virulence
  • Cell Movement
  • Phenotype
  • Models, Biological
  • Cellular Microenvironment
  • CD3 Complex