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Passive Administration of Monoclonal Antibodies Against H. capsulatum and Others Fungal Pathogens
09:57

Passive Administration of Monoclonal Antibodies Against H. capsulatum and Others Fungal Pathogens

Published on: February 14, 2011

Perforin is required for primary immunity to Histoplasma capsulatum

P Zhou1, B L Freidag, C C Caldwell

  • 1Clinical Immunology Section, Laboratory of Clinical Investigation, and Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|February 13, 2001
PubMed

Insights

Perforin plays a crucial role in controlling Histoplasma capsulatum (HC) infection, as shown by increased mortality in perforin-deficient mice. CD8(+) T cells also contribute to immunity against HC through both perforin-dependent and independent pathways.

Area of Science:

  • Immunology
  • Mycology
  • Infectious Diseases

Background:

  • Protective immunity against Histoplasma capsulatum (HC) involves innate and adaptive immune responses.
  • Interferon-gamma (IFN-gamma) and Tumor Necrosis Factor-alpha (TNF-alpha) are known to limit fungal growth.
  • The role of cytolytic mechanisms, such as perforin, in HC immunity is less understood.

Purpose of the Study:

  • To investigate the role of perforin in mediating immunity against primary and secondary Histoplasma capsulatum infections.
  • To explore the contribution of CD8(+) T cells to HC immunity, including perforin-dependent and independent mechanisms.

Main Methods:

  • Utilized perforin-deficient knockout (PfKO) mice and wild-type controls for challenge studies.
  • Depleted CD8(+) T cells in PfKO mice to assess their role.
  • Performed adoptive transfer of CD8(+) T cells from PfKO mice into IFN-gamma(-/-) mice.

Main Results:

  • Perforin-deficient mice exhibited accelerated mortality and increased fungal burden after HC challenge, highlighting perforin's essential role.
  • Depletion of CD8(+) T cells in PfKO mice exacerbated disease, suggesting perforin-independent CD8(+) T cell functions.
  • Adoptive transfer of CD8(+) T cells from PfKO mice reduced fungal burden in IFN-gamma(-/-) mice, indicating perforin-independent protective mechanisms.

Conclusions:

  • Perforin is critical for effective immunity against systemic Histoplasma capsulatum infection.
  • CD8(+) T cells contribute to Histoplasma capsulatum immunity through both perforin-dependent and independent pathways, with the latter being significant in the absence of IFN-gamma.

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