Cytokines produced by T helper (Th) cells are of critical importance for th
e outcome of many infectious diseases. Producing the "right" set of cytokin
es in response to an infectious agent can be a matter of life or death. The
Th1/Th2 dichotomy, although an oversimplification has proven useful in the
analysis of immune responses to infections. In some infectious diseases, m
ost notably leishmaniasis or infections with gastrointestinal helminths, on
e Th subset is indispensable for clearing the infection, whereas the opposi
te Th subset is detrimental. More frequently, both Th1 and Th2 responses ar
e required at different time points to effectively eradicate an infectious
agent. The granuloma responses to either Mycobacterium tuberculosis or Schi
stosoma mansoni provide illustrative examples and are discussed in this rev
iew. There is accumulating evidence for frequent coexpression of Th1 and Th
2 cytokines during the in vivo immune response to infections. The mechanism
s by which infectious agents modulate Th1/Th2 phenotype development are sum
marized here. Finally, we review here the current evidence for cytokine imb
alances induced by infections as pathogenic or protective factors in autoim
munity and allergy.