An inherent T cell deficit in healthy males to C. neoformans infection may begin to explain the sex susceptibility in incidence of cryptococcosis

Biol Sex Differ. 2019 Sep 2;10(1):44. doi: 10.1186/s13293-019-0258-2.

Abstract

Background: Cryptococcus neoformans, the causative agent of cryptococcosis, causes ~ 181,000 deaths annually, with males having a higher incidence of disease than females (7M:3F). The reason for this sex bias remains unclear. We hypothesized that this disparity was due to biological differences between the male and female immune response.

Methods: Peripheral blood mononuclear cells (PBMCs) from healthy donors were isolated and infected with C. neoformans ± exogenous testosterone or 17-β-estradiol. C. neoformans, B, T, and NK cell proliferation was quantified by flow cytometry. Cytokine analysis was conducted via protein array or ELISA. Serological testing was conducted to determine previous exposure to C. neoformans.

Results: C. neoformans proliferated more in male PBMCs. T cell percentages in both sexes were lower in infected versus uninfected cells. Male PBMCs had lower CD3+, CD4+, and CD8+ T cells percentages during infection compared to females. Cytokine profiles showed differences in uninfected male and female PBMCs, which subsided during infection. Only one donor was sero-negative for prior C. neoformans exposure. There was an effect of estrogen in one dataset.

Conclusions: These results suggest that males show an inherent deficit in T cell response during infection, which may contribute to the increased incidence of disease in males.

Keywords: B cells; Cryptococcosis; Cryptococcus neoformans; Estrogen; Immune response; Natural killer cells; Sex bias in infection; T cells; Testosterone.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Cell Proliferation
  • Cells, Cultured
  • Cryptococcosis / immunology*
  • Cryptococcus neoformans*
  • Cytokines / genetics
  • Cytokines / metabolism
  • Female
  • Humans
  • Interleukin-2 Receptor alpha Subunit / metabolism
  • Leukocytes, Mononuclear / microbiology*
  • Lymphocyte Count
  • Lymphocyte Subsets / metabolism
  • Lymphocyte Subsets / microbiology*
  • Male
  • Sex Characteristics

Substances

  • Cytokines
  • IL2RA protein, human
  • Interleukin-2 Receptor alpha Subunit