000 01637nam a2200193Ia 4500
003 MX-MdCICY
005 20250625122442.0
040 _cCICY
090 _aB-4519
245 1 0 _aImmune response to Leishmania infection
490 0 _vIndian Journal of Medical Research, 119, p.238-258, 2004
520 3 _aAntileishmanial immune response is shown to be host genotype dependent so that some inbred strains of mouse are susceptible while others are resistant. The resistance is conferred by T-helper type-1 (Th1)cells while the susceptibility is conferred by Th2 cells. Th1 cells secrete IL-2 and IFN-gamma but Th2 cells secrete IL-4, IL-5 and IL-10. It has been shown that IFN-gamma activates macrophages to express iNOS2, the enzyme catalyzing the formation of nitric oxide. Nitric oxide kills the intracellular amastigotes. In contrast, Th2 immune response limits the action of Th1 functions via IL-10 and IL-4, which deactivate macrophages helping intracellular parasite growth and disease progression. Being a parasite, Leishmania ensures its own survival by modulating host immune system either by inducing immunosuppression or by promoting pro-parasitic host functions. A detailed knowledge of this host-parasite interaction would help in designing prophylactic and therapeutic strategies against this infection.
700 1 2 _aAwasthi, A.
700 1 2 _aMathur, R. K.
700 1 2 _aSaha, B.
856 4 0 _uhttps://drive.google.com/file/d/1Z17ZRwP6z4cYQe8WY7l5EKxJkIcLBfga/view?usp=drivesdk
_zPara ver el documento ingresa a Google con tu cuenta: @cicy.edu.mx
942 _2Loc
_cREF1
008 250602s9999 xx |||||s2 |||| ||und|d
999 _c38884
_d38884