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Influence of HLA-DR2 on perforin-positive cells in pulmonary tuberculosis

D N Rajeswari1, P Selvaraj, S Raghavan

  • 1Tuberculosis Research Centre, Indian Council of Medical Research, Chetput, Chennai, India.

International Journal of Immunogenetics
|September 12, 2007
PubMed

Insights

Human leukocyte antigen (HLA)-DR2 may reduce perforin levels in cytotoxic T cells and natural killer cells, impacting pulmonary tuberculosis (PTB) progression. This finding highlights a potential genetic link in immune response to PTB.

Area of Science:

  • Immunogenetics
  • Cellular Immunology
  • Infectious Diseases

Background:

  • Perforin is a crucial molecule for cytotoxic T lymphocytes and natural killer cells.
  • Pulmonary tuberculosis (PTB) is a significant global health challenge.
  • The role of human leukocyte antigen (HLA) alleles in immune responses to PTB is not fully understood.

Purpose of the Study:

  • To investigate the influence of HLA-DRB1 alleles on perforin expression in immune cells.
  • To determine the association between HLA-DR2 and perforin levels in patients with PTB.

Main Methods:

  • Flow cytometry was used to quantify perforin-positive CD4, CD8, CD16, and CD56 cells.
  • HLA-DRB1 typing was performed using polymerase chain reaction-based sequence-specific oligonucleotide hybridization.
  • Study included normal healthy subjects (n=156) and PTB patients (n=102).

Main Results:

  • HLA-DR2-positive PTB patients showed significantly decreased percentages of total perforin-positive cells, CD8+/Per+, CD16+/Per+, and CD56+/Per+ cells compared to non-DR2 patients.
  • Among HLA-DR2 subtypes, DRB1*1501 showed a trend towards decreased CD16+/Per+ and CD56+/Per+ cells compared to DRB1*1502.
  • CD8+/Per+ cell percentages did not differ between DRB1*1501 and DRB1*1502.

Conclusions:

  • HLA-DR2 may be associated with the down-regulation of perforin in cytotoxic lymphocytes and natural killer cells in pulmonary tuberculosis.
  • This suggests a potential immunogenetic mechanism influencing disease susceptibility or progression in PTB.

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