Interferon-¿ and interleukin-4 in human Leishmania donovani infections

TY - JOUR

T1 - Interferon-¿ and interleukin-4 in human Leishmania donovani infections

AU - Kemp, M

AU - Kurtzhals, J A

AU - Kharazmi, A

AU - Theander, T G

N1 - Keywords: Animals; Humans; Immunity, Natural; Interferon Type II; Interleukin-4; Leishmania donovani; Leishmania major; Leishmaniasis, Cutaneous; Leishmaniasis, Visceral; Mice

PY - 1993

Y1 - 1993

N2 - Clinical and immunological similarities between Leishmania donovani infections in humans and L. major infections in mice suggest that some of the pathophysiological mechanisms are the same in the two conditions. Both infections can result either in a fatal systemic disease or in a self-limiting infection with few and mild symptoms. In the murine model the outcome of the infection is critically related to the cytokines produced by T lymphocytes activated by leishmanial antigens. Activation of the IFN-gamma producing Th1 subset of CD4 positive T cells results in cure and survival, whereas activation of the IL-4 secreting Th2 subset results in a progressive disease with fatal outcome. A similar Th1/Th2 dichotomy in the cytokine response to L. donovani may exist in humans, and may have influence on the outcome of infection. In murine leishmaniasis the levels of IL-4 and IFN-gamma at the time of infection can direct the T cell response into Th1 or Th2 type. If similar mechanisms operate in humans, the outcome of L. donovani infections may depend on the local cytokine environment in which early activation of Leishmania specific T cells takes place. Cytokines secreted by cross-reactive memory T cells, activated by antigens from the invading micro-organism, may contribute to determine this environment.

AB - Clinical and immunological similarities between Leishmania donovani infections in humans and L. major infections in mice suggest that some of the pathophysiological mechanisms are the same in the two conditions. Both infections can result either in a fatal systemic disease or in a self-limiting infection with few and mild symptoms. In the murine model the outcome of the infection is critically related to the cytokines produced by T lymphocytes activated by leishmanial antigens. Activation of the IFN-gamma producing Th1 subset of CD4 positive T cells results in cure and survival, whereas activation of the IL-4 secreting Th2 subset results in a progressive disease with fatal outcome. A similar Th1/Th2 dichotomy in the cytokine response to L. donovani may exist in humans, and may have influence on the outcome of infection. In murine leishmaniasis the levels of IL-4 and IFN-gamma at the time of infection can direct the T cell response into Th1 or Th2 type. If similar mechanisms operate in humans, the outcome of L. donovani infections may depend on the local cytokine environment in which early activation of Leishmania specific T cells takes place. Cytokines secreted by cross-reactive memory T cells, activated by antigens from the invading micro-organism, may contribute to determine this environment.

M3 - Journal article

C2 - 8314285

SN - 0818-9641

VL - 71 ( Pt 6)

SP - 583

EP - 587

JO - Immunology and Cell Biology

JF - Immunology and Cell Biology

ER -