Expansion of the gamma delta T cell subset in vivo during bloodstage malaria in B cell-deficient mice

• Published in: Journal of leukocyte biology Vol. 60; no. 2; pp. 221 - 229
• Main Authors: Van der Heyde, HC, Elloso, M M, Chang, Wun-Ling, Pepper, B J, Batchelder, J, Weidanz, W P
• Format: Journal Article
• Language: English
• Published: 01-08-1996
• ISSN: 0741-5400
• DOI: 10.1002/jlb.60.2.221

Mice rendered B cell-deficient either by chronic anti- mu treatment initiated at birth or by gene knockout (JHD and mu -MT mice) suppressed acute Plasmodium chabaudi infections with a time course similar to intact control mice. Moreover, both kinds of B cell-deficient mice showed a 50- to 100-fold increase in splenic gamma delta T cell number after suppression of parasitemia compared with uninfected B cell-deficient controls; the magnitude of this increase resulted in significantly (P < 0.05) greater numbers of splenic gamma delta T cells in the B cell-deficient mice than in infected B cell-intact controls (about 10-fold). In contrast, the number of splenic CD4 super(+) alpha beta T cells was only slightly elevated (< 2-fold) in both kinds of B cell-deficient mice compared with their intact controls. The number of splenic gamma delta T cells following suppression of P. vinckei parasitemia was approximately ninefold greater in JHD mice than in C57BL/6 controls, whereas similar numbers of splenic CD4 super(+) alpha beta T cells were detected. Maximal numbers of gamma delta T cells were in cell-cycle in both JHD and C57BL/6 mice during descending P. chabaudi parasitemia, but the number of gamma delta T cells in cell-cycle was greater in B cell-deficient mice than in intact controls. Interleukin-10 (IL-10), a potent T sub(H1) cell-suppressive molecule, does not appear to down-regulate the gamma delta T cell response during malaria in B cell-intact mice because the magnitude of the gamma delta T cell response was not significantly greater in IL-10 knockout mice compared with heterozygote controls. These findings collectively indicate that a markedly enhanced expansion of the gamma delta T cell population occurs in the absence of B cells, and this expansion occurs predominantly during acute malaria when parasite burdens are similar in B cell-deficient animals and intact controls.