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[Immune response in dermatophytosis].

Tetsuya Koga1

  • 1Department of Dermatology, Fukuoka Red Cross Hospital, 3-1-1 Ookusu, Minami-ku, Fukuoka 815-8555, Japan.

Nihon Ishinkin Gakkai Zasshi = Japanese Journal of Medical Mycology
|November 15, 2003
PubMed
Summary

The study shows that a Th1 immune response, involving interferon-gamma (IFN-gamma), is crucial for fighting fungal skin infections like dermatophytosis. This response, however, does not seem to be deficient in patients with tinea unguium.

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[Fungal immunology in the skin; immune response to dermatophytes].

Nihon Ishinkin Gakkai zasshi = Japanese journal of medical mycology·2009

Area of Science:

  • Immunology
  • Dermatology
  • Mycology

Context:

  • Dermatophytosis, a fungal skin infection, involves complex host immune responses.
  • The role of T-helper 1 (Th1) cell-mediated immunity, characterized by interferon-gamma (IFN-gamma) production, is investigated in the context of dermatophyte infections.
  • Keratinocytes' role in initiating inflammatory responses to fungal antigens is explored.

Purpose:

  • To investigate the host immune response, specifically the Th1 response and keratinocyte involvement, in dermatophytosis.
  • To determine if a deficiency in the Th1 response to dermatophyte antigens contributes to the development of tinea unguium.

Summary:

  • Peripheral blood mononuclear cells from patients with dermatophytosis exhibit a robust Th1 response, evidenced by high IFN-gamma production upon stimulation with trichophytin.
  • IFN-gamma mRNA and IFN-gamma-positive cells are detected in skin lesions, supporting the association of Th1 responses with cutaneous reactions in dermatophytosis.
  • Trichophytin stimulates keratinocytes to release IL-8, suggesting a role for keratinocytes in initiating acute inflammation and host defense against dermatophytes.
  • Patients with tinea unguium do not show a deficiency in IFN-gamma production or lymphocyte proliferation in response to trichophytin, indicating that a compromised Th1 response is unlikely to be a primary factor in disease establishment.

Impact:

  • These findings highlight the significant role of Th1 immunity and keratinocyte-derived IL-8 in the host defense against dermatophytes.
  • The study suggests that keratinocytes contribute to initiating cutaneous inflammatory reactions, acting as more than just a physical barrier.
  • The research indicates that a deficient Th1 response is not a major factor in the pathogenesis of tinea unguium, redirecting focus to other potential mechanisms.

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