The influence of γδ T cells on the CD4+ T cell and antibody response during a primary Plasmodium chabaudi chabaudi infection in mice
The influence of γδ T cells on the CD4+ T cell and antibody response during a primary Plasmodium chabaudi chabaudi infection in mice
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DOI：
10.1046/j.1365-3024.2002.00446.x
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发表时间：
2002-03-01
影响因子：
2.2
通讯作者：
Langhorne, J
中科院分区：
文献类型：
--
作者：
Seixas, E;Fonseca, L;Langhorne, J
A primary infection with Plasmodium chabaudi chabaudi (AS) is characterized by an expansion of gammadeltacells after the acute phase of infection in mice. This is particularly marked during chronic infections in B cell-deficient mice. Infections in gammadeltaT cell-deficient mice suggest that, although these cells play some role in the control of parasitaemia and can produce interferon- gamma, they do not appear to be involved in the development of hypoglycaemia, loss of weight and temperature during a P. c. chabaudi infection. However, gammadeltaT cells do influence the nature of the CD4(+) T cell response during infection since, in their absence, Th2-like responses, such as interleukin (IL)-4 production and help for malaria-specific antibody responses, are more pronounced. This alteration in CD4(+) T cells is reflected in a more rapid and greater immunoglobulin (Ig)G1 and IgG3 antibody response to the parasite. The large gammadeltaT cell expansion normally observed in infected B cell-deficient mice did not take place in the absence of IL-2, and double-knockout mice lacking both B cells and functional IL-2 were highly susceptible to lethal infection with P. c. chabaudi. The majority of the single IL-2 knockout mice, in contrast, were able to control and clear a primary infection, suggesting that for the CD4(+) T cell and antibody response, IL-2 could be replaced by other cytokines.
