Immune activation requires a signal when circulating blood is used as the cell source, since the peripheral-blood lymphocyte is a resting cell. This signal is often a plant lectin, or another signal, such as certain divalent cations, calcium ionophores or surface-reactive molecules, including monoclonal antibodies to CD3, which provide a non-antigenic stimulus that activates T lymphocytes independently of antigenic history. Impaired response to mitogens in human settings of PEM may or may not be accompanied by loss of response to pathogens. Examples include the study of response to PPD in malnourished children at risk of tuberculosis and the effect of stunting on the response to malarial antigens (discussed above). It is well known that infections with even relatively non-pathogenic viruses, such as measles, are often fatal in children with PEM, because measles-virus infection causes a serious but usually transient suppression of the cellular immune response (Schlender et al., 1996; Ito et al., 1997), which, in the malnourished host, may continue to prevent immune clearance. Longitudinal studies are often essential to demonstrate long-term effects, such as the lingering effect of vitamin A deficiency, which increases mortality from infections (West et al., 1999). Current studies suggest that the specificity of the response, defined as a Th1 or Th2 cytokine-pattern, to a specific microbe is critically associated with host defence. Study designs that incorporate antigens that are actually being encountered at the time of study or that focus on the type of cytokine production may therefore provide important and unique information.
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