Dichotomy in the human CD4⁺ T-cell response to Leishmania parasites

TY - JOUR

T1 - Dichotomy in the human CD4+ T-cell response to Leishmania parasites

AU - Kemp, M

AU - Kurtzhals, J A

AU - Kharazmi, A

AU - Theander, T G

N1 - Keywords: Animals; Antigens, CD; Antigens, CD4; CD4-Positive T-Lymphocytes; Humans; Immunity, Cellular; Interferon Type II; Leishmania; Leishmaniasis; Mice

PY - 1994

Y1 - 1994

N2 - Leishmania parasites cause human diseases ranging from self-healing cutaneous ulcers to fatal systemic infections. In addition, many individuals become infected without developing disease. In mice the two subsets of CD4+ T cells, Th1 and Th2, have different effects on the outcome of experimental Leishmania infections. Th1 cells producing interferon-gamma (IFN-gamma) mediate resistance, whereas Th2 cells producing interleukin-4 (IL-4) and IL-10 are associated with susceptibility and exacerbation. Evidence is accumulating that a Th1/Th2 dichotomy in the T-cell response to Leishmania exists also in humans, and that the balance between subsets of parasite-specific T cells may play an important regulatory role in determining the outcome of the infections.

AB - Leishmania parasites cause human diseases ranging from self-healing cutaneous ulcers to fatal systemic infections. In addition, many individuals become infected without developing disease. In mice the two subsets of CD4+ T cells, Th1 and Th2, have different effects on the outcome of experimental Leishmania infections. Th1 cells producing interferon-gamma (IFN-gamma) mediate resistance, whereas Th2 cells producing interleukin-4 (IL-4) and IL-10 are associated with susceptibility and exacerbation. Evidence is accumulating that a Th1/Th2 dichotomy in the T-cell response to Leishmania exists also in humans, and that the balance between subsets of parasite-specific T cells may play an important regulatory role in determining the outcome of the infections.

M3 - Journal article

C2 - 7909443

SN - 0903-465X

VL - 102

SP - 81

EP - 88

JO - APMIS. Supplementum

JF - APMIS. Supplementum

IS - 2

ER -