When the body's own cells become infected, the immune system can take the extreme step of killing them to preserve the rest of the organism. It is no surprise that this potentially dangerous mechanism has to be kept under strict control, and onpages 474¹,478² and480³ of this issue, three groups suggest a new mechanism by which this control operates.

The need for helpers and the nature of this help have intrigued immunologists for years. The first model (Fig. 1b) suggested that T-helper and T-killer cells recognize their specific antigens simultaneously on the same APC, and that cytokines (such as interleukin-2) produced by the activated T-helper cell would act on the T killer and facilitate its response⁴,⁵. Although interleukin-2 can substitute for helper cells in some systems, there are two main problems with this model. First, it requires that two rare antigen-specific cells meet on the same antigen-bearing APC — an event that has an extremely low probability. Second, and more importantly, some killer responses can be elicited in the absence of helper cells⁶, implying that the need for help is conditional rather than absolute.

This is a preview of subscription content,access via your institution